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Different Types of Antibodies, Production and Functions

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Different Types of Antibodies, Production and Functions

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Different type of immune deficiency and example and mechanism

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Different type of immune deficiency and example and mechanism

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Factors that affect secondary immune response

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Factors that affect secondary immune response

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Interaction of Antigen Presenting Cells and T-helper Cells

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T-cell Deoendent antigens , immunology , T-helper Cells

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B and T lymphocyte, dendritic cells will be situated mainly in the germinal centre of the cortex of lymph nodes. Some will be scattered around the cortex sinus. Plasma cells will be situated in the medullary cord

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- activate complement system
- first immunoglobulin secreted
- coexpressed with IgD
- formed pentamer by J chain
- max 5 binding sites( Fab ) due to conformational constraint
- short half life
- promote lysis
- only immunoglobulin synthesized by foetus
- in Fc region

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Function
- Filter lymph of harmful pathogens such as bacteria or viruses

- Assist the immune system in building an immune response

- House of lymphocytes (B cell and T cell)

- B-cell lymphocytes become activated due to presence of antigen – release of antibodies

- T-cell lymphocytes responsible for cell mediated immunity and destruction of pathogens

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- serum
- body fluid
- monomer
- long half life
- 4 subtypes: IgG1, IgG2, IgG3, IgG4
- IgG long hlaf life except IgG3
- bind to macrophage Fc receptor by IgG1, IgG3
- activate complement
- class switch with IgM
- cross placenta( IgG2 is less efficient in crossing placenta)

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A number of rare diseases feature a heightened susceptibility to infections from childhood onward. Primary Immunodeficiency is also known as congenital immunodeficiencies. Many of these disorders are hereditary and are autosomal recessive or X-linked. There are over 80 recognised primary immunodeficiency syndromes; they are generally grouped by the part of the immune system that is malfunctioning, such as lymphocytes or granulocytes. The treatment of primary immunodeficiencies depends on the nature of the defect, and may involve antibody infusions, long-term antibiotics and (in some cases) stem cell transplantation.

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Secondary immunodeficiencies, also known as acquired immunodeficiencies, can result from various immunosuppressive agents, for example, malnutrition, aging, particular medications (e.g., chemotherapy, disease-modifying antirheumatic drugs, immunosuppressive drugs after organ transplants, glucocorticoids) and environmental toxins like mercury and other heavy metals, pesticides and petrochemicals like styrene, dichlorobenzene, xylene, and ethylphenol. For medications, the term immunosuppression generally refers to both beneficial and potential adverse effects of decreasing the function of the immune system, while the term immunodeficiency generally refers solely to the adverse effect of increased risk for infection.  Many specific diseases directly or indirectly cause immunosuppression. This includes many types of cancer, particularly those of the bone marrow and blood cells (leukemia, lymphoma, multiple myeloma), and certain chronic infections. Immunodeficiency is also the hallmark of acquired immunodeficiency syndrome (AIDS), caused by the human immunodeficiency virus (HIV). HIV directly infects a small number of T helper cells, and also impairs other immune system responses indirectly.  Various hormonal and metabolic disorders can also result in immune deficiency including anemia, hypothyroidism, diabetes and hypoglycemia.  Smoking, alcoholism and drug abuse also depress immune response.

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Immunodeficiency related to Autoimmunity 

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Immunodeficiency related to Autoimmunity 

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There are a large number of immunodeficiency syndromes that present clinical and laboratory characteristics of autoimmunity. The decreased ability of the immune system to clear infections in these patients may be responsible for causing autoimmunity through perpetual immune system activation. One example is common variable immunodeficiency (CVID) where multiple autoimmune diseases are seen, e.g., inflammatory bowel disease, autoimmune thrombocytopenia and autoimmune thyroid disease. Familial hemophagocytic lymphohistiocytosis, an autosomal recessive primary immunodeficiency, is another example. Pancytopenia, rashes, lymphadenopathy and hepatosplenomegaly are commonly seen in these patients. Presence of multiple uncleared viral infections due to lack of perforin are thought to be responsible. In addition to chronic and/or recurrent infections many autoimmune diseases including arthritis, autoimmune hemolytic anemia, scleroderma and type 1 diabetes are also seen in X-linked agammaglobulinemia (XLA). Recurrent bacterial and fungal infections and chronic inflammation of the gut and lungs are seen in chronic granulomatous disease (CGD) as well. CGD is caused by a decreased production of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase by neutrophils. Hypomorphic RAG mutations are seen in patients with midline granulomatous disease; an autoimmune disorder that is commonly seen in patients with granulomatosis with polyangiitis (Wegner’s disease) and NK/T cell lymphomas. Wiskott-Aldrich syndrome (WAS) patients also present with eczema, autoimmune manifestations, recurrent bacterial infections and lymphoma. In autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) also autoimmunity and infections coexist: organ-specific autoimmune manifestations (e.g., hypoparathyroidism and adrenocortical failure) and chronic mucocutaneous candidiasis. Finally, IgA deficiency is also sometimes associated with the development of autoimmune and atopic phenomena.

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Total white cell count: 4-11 * 10^9 l
Neutrophil: 2-7.5 * 10^9 l
Lymphocyte: 1.5-4 * 10^9 l
Monocyte: 0.2-0.8 * 10^9 l
Eosinophil: 0.04-0.4 * 10^9 l
Basophil: 0.01-0.1 * 10^9 l

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Neutrophil: 40-80%
Lymphocyte: 20-40%
Monocyte: 2-10%
Eosinophil: 1-6%
Basophil: <1-2%

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Differential blood count gives relative percentage of each type of white blood cell and also helps reveal abnormal white blood cell populations (eg, blasts, immature granulocytes, or circulating lymphoma cells in the peripheral blood).

Differential blood count is also used along with leukocyte count (WBC) to generate an absolute value for each type of white blood cells (eg, absolute neutrophil count, absolute lymphocyte count, or absolute eosinophil count), which usually gives more meaningful information than the percentage of each, since relative percentage can be misleading. Expressing absolute values are also useful for monitoring (eg, monitoring neutropenia during chemotherapy or bone marrow transplantation). [¹] Using absolute values, conditions such as neutropenia, neutrophilia, lymphopenia, lymphocytosis, monocytopenia, monocytosis, eosinophilia, and basophilia can be identified, whichcanhelp differential diagnosis of patient’s underlying disorders.

Differential blood count is not a part of complete blood count (CBC) but is interpreted together with CBC to help support or exclude a suspected diagnosis. For example, the presence of anemia along with thrombocytopenia with a low or high white blood cell count may suggest bone marrow involvement by leukemia

Source: Medscape

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Review of B cells, CD4+ T cells and CD8+ T cells | NCLEX-RN | Khan Academy

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Malnutrition (unbalanced diet/poor eating habits that cause a lack of vitamins and minerals)

· Alcohol abuse

· Drug abuse, either intravenous or other (appears related to associated factors i.e. poor diet, use of infected/dirty needles, poor exercise, stress/depression)

· Medications (particularly the use of anti-cancer drugs, corticosteroids, and antibiotics)

· Radiation

· Exposure to certain environmental toxins, whether naturally occurring or from pollution. These include:

· Cigarette smoke

· Stress/Depression - Research shows that psychological stress can greatly increase your susceptibility to colds and other viral diseases, namely through an increase in serum corticosteroid levels

· Age - Ability of the immune system to respond is decreased at early and old age.

· Disease or medications (i.e. Diabetes, corticosteroids, immune suppressant drugs), causing constant exposure to infectious agents without natural defense (intact skin)

· Inadequate sleep at the Delta brain wave level.

· Lack of exercise as well as excessive exercise resulting in physiological stress

· Long-term weightlessness

· Diseases either infectious or other causing more depression on the immune system like:

o Cancer, and hematological malignancy (such as leukemia, lymphoma and myeloma) in particular.

o Diabetes Mellitus

o Cystic fibrosis

o Lupus Erythematosus

o Nephrotic syndrome

o Viral infections i.e. viral respiratory infections then allowing for bacterial pneumonia to develop.

o HIV

o Ulcerative colitis

o Bulimia (due to malnutrition, stress, depression).

o Sickle-cell disease.

o Liver disease/cirrhosis

o Cushing's syndrome

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a.       Disease control benefit
i.      Eradication: Unless an environmental reservoir exists, an eradicated pathogen cannot re-emerge, unless accidentally or malevolently reintroduced by humans, allowing vaccination or other preventive measures to be discontinued. While eradication may be an ideal goal for an immunization programme, to date only smallpox has been eradicated, allowing discontinuation of routine smallpox immunization globally. Potentially, other infectious diseases with no extrahuman reservoir can be eradicated provided an effective vaccine and specific diagnostic tests are available. Eradication requires high levels of population immunity in all regions of the world over a prolonged period with adequate surveillance in place. The next disease targeted for eradication is polio, which is still a global challenge. Although high coverage with oral polio vaccine (OPV) has eliminated type 2 poliovirus globally, transmission of types 1 and 3 continues in limited areas in a few countries. OPV-caused paralytic disease, directly or by reversion to virulence, and persistent vaccine-virus excretion in immunodeficient individuals are problems yet to be solved. Global use of monovalent type 1 and type 3 OPV and inactivated polio vaccine (IPV) may eventually be required.

ii.      Elimination

Diseases can be eliminated locally without global eradication of the causative microorganism. In four of six WHO regions, substantial progress has been made in measles elimination; transmission no longer occurs indigenously and importation does not result in sustained spread of the virus. Key to this achievement is more than 95% population immunity through a two-dose vaccination regimen. Combined measles, mumps and rubella (MMR) vaccine could also eliminate and eventually eradicate rubella and mumps. Increasing measles immunization levels in Africa, where coverage averaged only 67% in 2004, is essential for eradication of this disease. Already, elimination of measles from the Americas, and of measles, mumps and rubella in Finland has been achieved, providing proof in principle of the feasibility of their ultimate global eradication. It may also be possible to eliminate Haemophilus influenzae type b (Hib) disease through well implemented national programmes, as experience in the West has shown.

Local elimination does not remove the danger of reintroduction, such as in Botswana, polio-free since 1991, with importation of type 1 poliovirus from Nigeria in 2004, and in the United States of America (USA) with measles reintroduced to Indiana in 2005 by a traveller from Romania.

For diseases with an environmental reservoir such as tetanus, or animal reservoirs such as Japanese encephalitis and rabies, eradication may not be possible, but global disease elimination is a feasible objective if vaccination of humans (and animals for rabies) is maintained at high levels.

b.       Control of mortality, morbidity and complications

i.      Efficacious vaccines protect individuals if administered before exposure. Pre-exposure vaccination of infants with several antigens is the cornerstone of successful immunization programmes against a cluster of childhood diseases. Vaccine efficacy against invasive Hib disease of more than 90% was demonstrated in European, Native American, Chilean and African children in large clinical studies in the 1990s. In the United Kingdom, no infant given three doses developed Hib disease in the short-term (boosters may be required for long-term protection), and recent postmarketing studies have confirmed the high effectiveness of vaccination of infants against Hib in Germany and pertussis in Sweden.

ii.      Many vaccines can also protect when administered after exposure – examples are rabies, hepatitis B, hepatitis A, measles and varicella.

c.       Mitigation of disease

i.      Disease may occur in previously vaccinated individuals. Such breakthroughs are either primary – due to vaccine failure – or secondary. In such cases, the disease is usually milder than in the non-vaccinated. In a German efficacy study of an acellular pertussis vaccine, vaccinated individuals who developed whooping cough had a significantly shorter duration of chronic cough than controls. Such findings were confirmed in Senegal. Varicella breakthroughs exhibit little fever, fewer skin lesions and fewer complications than unvaccinated cases. Milder disease in vaccinees was also reported for rotavirus vaccine.

d.       Prevention of infection
i.      Many vaccines are primarily intended to prevent disease and do not necessarily protect against infection. Some vaccines protect against infection as well. Hepatitis A vaccine has been shown to be equally efficacious (over 90% protection) against symptomatic disease and asymptomatic infections. Complete prevention of persistent vaccine-type infection has been demonstrated for human papillomavirus (HPV) vaccine. Such protection is referred to as “sterilizing immunity”. Sterilizing immunity may wane in the long term, but protection against disease usually persists because immune memory minimizes the consequences of infection

e.       Protection of the unvaccinated population

i.      Efficacious vaccines not only protect the immunized, but can also reduce disease among unimmunized individuals in the community through “indirect effects” or “herd protection”.

ii.      “Herd protection” of the unvaccinated occurs when a sufficient proportion of the group is immune. The decline of disease incidence is greater than the proportion of individuals immunized because vaccination reduces the spread of an infectious agent by reducing the amount and/or duration of pathogen shedding by vaccinees, retarding transmission.

f.        Prevention of related diseases and cancer

i.      Vaccines will also protect against diseases related to the targeted disease. For example, in Finland, the USA and elsewhere, influenza vaccination has been found protective for acute otitis media in children, with a vaccine efficacy of more than 30%. Measles vaccination protects against multiple complications such as dysentery, bacterial pneumonia, keratomalacia and malnutrition.An enterotoxic Escherichia coli vaccine demonstrated protection against diarrhoea due to Salmonella enterica.

ii.      infective agents cause several cancers. Chronic hepatitis B infection leads to liver cancer. Vaccination against such pathogens should prevent the associated cancer as already observed for hepatocellular carcinoma. Reduction of the incidence of cervical cancer is expected with the use of HPV vaccines against serotypes 16 and 18, responsible for over 70% of the global cervical cancer burden, as reduction in precancerous lesions has been demonstrated in vaccinees.

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A video about vaccines.

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How do vaccines work? - Kelwalin Dhanasarnsombut

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The Importance of Immunization - Xpress Urgent Care

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Getting immunized is an important aspect of maintaining a healthy body, but not everyone appreciates the importance of vaccination. Vaccines defend against preventable diseases that can cause a number of serious complications, including amputation of major body parts, limb paralysis, hearing loss, convulsions, brain damage, and even death.

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-          First step in initiation of the immune response to an antigen must necessarily involve modification of the antigen, and these specialized cells are called APCs

-          Without this, T cells cannot recognise the antigen

-          The secretion of cytokines by APCs activated by antigen presentation that further activates antigen-specific T cells

-          This interaction between APCs and T cells is strongly influenced by a group of molecules called co-stimulators

-          The absence of co-stimulators leads to T-cell unresponsiveness

-          Processed antigen is presented to the T cells in the context of the MHC complex present on the surface of APCs

-          Most efficient APCs are the dendritic cells.

-          These dendritic cells have high concentrations of MHC class I and II antigens, co-stimulatory molecules, and adhesion molecules on their surface

-          Dendritic cells on the skin – Langerhans cells = important role in immune defences, mobile, can capture antigen in the periphery and migrate to secondary lymph nodes where dendritic cells become mature and interact with naïve T cells

-          The follicular dendritic cells reside in the follicular germinal center (B-cell area) of a lymph node

-          These cells have receptors for complement and immunoglobulins and their function is to trap immune complexes and feed them to B cells

-          Closely associated with MHC class II molecules on the APC surfaces and thus activates B cells

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Factors affecting antibody production(start from Slide 17)

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Factors affecting antibody production(start from Slide 17)

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There is a capsule surrounding the lymph node with sub capsular sinus situated beneath the capsule and there are also intermediate sinuses (sub capsular sinus which projects inwards)
In the outer cortex there are lymphoid nodules, some are primary and some are secondary. Secondary lymphoid nodules have a pale centre area representing the germinative centres. These centres are absent in primary lymphoid nodules.

In the medulla, there are medullary cords which are separated by medullary sinuses. Here, lymphocytes predominate however in the medullary cords, there are also plasma cells and blood vessels

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Features Running on Empty
Regularly taking breaks from eating-for hours or days-can trigger changes both expected, such as in metabolic dynamics and inflammation, and surprising, as in immune system function and cancer progression.

Notebook Athletes' Microbiomes Differ from Nonathletes
Researchers are beginning to uncover a link between activity level and the microbial makeup of one's gut.

Daily News Stomach Cells Change Identity to Drive Precancerous State
A study suggests that "chief" cells in the stomach act as reserve stem cells that are activated by tissue damage and may be the long-sought source of gastric cancer.

The Nutshell Mutation Linked to Longer Life Span in Men
A deletion in a growth hormone receptor gene is tied to an average of 10 extra years of life among men, but not women, according to a study.

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European Court OKs Vaccine Lawsuits Lacking Proof | The Scientist Magazine®

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Features Running on Empty Regularly taking breaks from eating-for hours or days-can trigger changes both expected, such as in metabolic dynamics and inflammation, and surprising, as in immune system function and cancer progression. Notebook Athletes' Microbiomes Differ from Nonathletes Researchers are beginning to uncover a link between activity level and the microbial makeup of one's gut.

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Myeloma cells result in the production of abnormal antibodies, or M proteins. A high level of M protein in the blood is the hallmark characteristic of multiple myeloma. Additionally, all myeloma cells are identical to each other and produce large quantities of the same specific M protein (for example, IgG or IgA). The M proteins offer no benefit to the body, and as the amount of M protein increases, it crowds out normally functioning immunoglobulins. This ultimately causes multiple myeloma symptoms such as bone damage or kidney problems.

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As the myeloma cells grow in excess, they disrupt normal cell production, which can result in numerous health complications. The exact complications of multiple myeloma will vary by individual; however, multiple myeloma primarily affects the bones, the blood and the kidneys.

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Bone pain with lytic lesions discovered on routine skeletal films or other imaging modalities

●An increased total serum protein concentration

and/or the presence of a monoclonal protein in the urine or serum

●Systemic signs or symptoms suggestive of malignancy, such as unexplained anemia

●Hypercalcemia, which is either symptomatic or discovered incidentally

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Blood tests. Laboratory analysis of your blood may reveal the M proteins produced by myeloma cells. Another abnormal protein produced by myeloma cells — called beta-2-microglobulin — may be detected in your blood and give your doctor clues about the aggressiveness of your myeloma.

Additionally, blood tests to examine your kidney function, blood cell counts, calcium levels and uric acid levels can give your doctor clues about your diagnosis.

Urine tests. Analysis of your urine may show M proteins, which are referred to as Bence Jones proteins when they're detected in urine.

Examination of your bone marrow. Your doctor may remove a sample of bone marrow for laboratory testing. The sample is collected with a long needle inserted into a bone (bone marrow aspiration and biopsy).

In the lab, the sample is examined for myeloma cells. Specialized tests, such as fluorescence in situ hybridization (FISH) can analyze myeloma cells to understand their chromosome abnormalities. Tests are also done to measure the rate at which the myeloma cells are dividing.

Imaging tests. Imaging tests may be recommended to detect bone problems associated with multiple myeloma. Tests may include X-ray, MRI, CT or positron emission tomography (PET).

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For decades the diagnosis of multiple myeloma required the presence of end-organ damage known as the CRAB criteria, including increased calcium level, renal dysfunction, anemia, and destructive bone lesions.

The updated criteria allow for treatment of patients who are at such high risk of progression to symptomatic disease that it is clear they would benefit from therapy and also potentially live longer if they were treated before serious organ damage occurred.

The revised IMWG criteria allow, in addition to the classic CRAB features, three myeloma defining events (MDEs). The presence of at least one of these markers is considered sufficient for a diagnosis of multiple myeloma, regardless of the presence or absence of symptoms or CRAB features. Each of these markers has been shown in two or more independent studies to be associated with an approximately 80% or higher risk of developing myeloma-related organ damage within two years.

The new definition of active multiple myeloma is:

Clonal bone marrow plasma cells 10% or biopsy-proven bony or extramedullary plasmacytoma and any one or more of the following CRAB features and myeloma-defining events:

Evidence of end organ damage that can be attributed to the underlying plasma cell proliferative disorder, specifically:

Hypercalcemia: serum calcium >0.25 mmol/L (>1mg/dL) higher than the upper limit of normal or >2.75 mmol/L (>11mg/dL)

Renal insufficiency: creatinine clearance <40 mL per minute or serum creatinine >177�mol/L (>2mg/dL)

Anemia: hemoglobin valure of >20g/L below the lowest limit of normal, or a hemoglobin value <100g/L

Bone lesions: one or more osteolytic lesion on skeletal radiography, CT, or PET/CT.� If bone marrow has <10% clonal plasma cells, more than one bone lesion is required to distinguish from solitary plasmacytoma with minimal marrow involvement

Any one or more of the following biomarkers of malignancy (MDEs):

60% or greater clonal plasma cells on bone marrow examination

Serum involved / uninvolved free light chain ratio of 100 or greater, provided the absolute level of the involved light chain is at least 100mg/L (a patients involved free light chain either kappa or lambda is the one that is above the normal reference range; the uninvolved free light chain is the one that is typically in, or below, the normal range)

More than one focal lesion on MRI that is at least 5mm or greater in size.

Recommended exam, tests, and imaging studies for the diagnosis of myeloma

1. History and Physical Examination

2. Routine Testing

Complete blood count with differential and peripheral blood smear review

Chemistry panel including calcium and creatinine

Serum protein electrophoresis, immunofixation

Nephelometric quantitation of immunoglobulins

Routine urinalysis, 24h urine collection for proteinuria,�electrophoresis and immunofixation

Quantification of both urine M-component level and albuminuria

3. Bone Marrow Testing: Obtain an aspirate plus trephine biopsy with testing for cytogenetics, fluorescent in situ hybridization (FISH) and immunophenotyping.

4. Imaging

Bone survey including spine, pelvis, skull, humeri and femurs.

The IWMG now recommends the use of low-dose whole-body CT (LDWBCT) or MRI in the work-up of smoldering multiple myeloma (SMM) and solitary plasmacytoma.

The IMWG now recommends that one of PET-CT, LDWBCT, or MRI of the whole body or spine be done in all patients with suspected smoldering myeloma, with the exact imaging modality determined by availability and resources.

Clear evidence of one or more sites of osteolytic bone destruction (?5mm in size) seen on CT (including LDWBCT) or PET-CT does fulfill the criteria for bone disease in multiple myeloma, and should be regarded as meeting the CRAB requirement irrespective of whether the lesions can be visualized on skeletal radiography or not.

Increased uptake on PET-CT alone is not adequate for the diagnosis of multiple myeloma; evidence of underlying osteolytic bone destruction is needed on the CT portion of the examination.

Bone densitometry studies are not sufficient to determine presence of multiple myeloma.

The IMWG no longer recommends the presence of osteoporosis or vertebral compression fractures in the absence of lytic lesions as being sufficient evidence of bone disease for purposes of the diagnostic criteria.

http://imwg.myeloma.org/international-myeloma-working-group-imwg-criteria-for-the-diagnosis-of-multiple-myeloma/

https://www.themmrf.org/multiple-myeloma/diagnosis/diagnostic-criteria/

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A myeloma protein is an abnormal immunoglobulin fragment or immunoglobulin light chain that is produced in excess by an abnormal monoclonal proliferation of plasma cells, typically in multiple myeloma. Other terms for such a protein are M protein, M component, spike protein, or paraprotein. This proliferation of the myeloma protein has several deleterious effects on the body, including impaired immune function, abnormally high viscosity ("thickness") of the blood, and kidney damage. Myeloma is a malignancy of the plasma cell. Plasma cells produce immunoglobulins, which are commonly called antibodies. There are thousands of different antibodies, each consisting of pairs of heavy and light chains. Antibodies are typically grouped into five types: IgA, IgD, IgE, IgG, and IgM. When someone contracts myeloma, a malignant clone, a rogue plasma cell, reproduces in an uncontrolled fashion, resulting in overproduction of the specific antibody the original cell was generated to produce. Each type of antibody has a different number of light chain and heavy chain pairs. As a result, there is a characteristic normal distribution of these antibodies in the blood by molecular weight. When there is a malignant clone, there is usually overproduction of a single antibody, resulting in a "spike" on the normal distribution, which is called an M spike (or monoclonal spike). People will sometimes develop a condition called MGUS (Monoclonal gammopathy of undetermined significance), where there is overproduction of one antibody but the condition is benign (does not threaten the patient's health). An explanation of the difference between multiple myeloma and MGUS can be found in the International Myeloma Foundation's Patient Handbook and Concise Review. Detection of paraproteins in the urine or blood is most often associated with benign monoclonal gammopathy of undetermined significance (MGUS), where they remain "silent", and multiple myeloma. An excess in the blood is known as paraproteinemia. Paraproteins form a narrow band, or 'spike' in protein electrophoresis as they are all exactly the same protein. Unlike normal immunoglobulin antibodies, paraproteins cannot fight infection. Serum free light-chain measurement can detect free light chains in the blood. Monoclonal free light chains in the serum or urine are called Bence Jones proteins.Blood serum paraprotein levels of more than 30 g/L is diagnostic of multiple myeloma, according to the diagnostic criteria of the International Myeloma Working Group.Detection of paraprotein in serum of less than 30 g/L is classified as monoclonal gammopathy of undetermined significance in cases where clonal plasma cells constitute less than 10% on bone marrow biopsy and there is no myeloma-related organ or tissue impairment.

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Diagnosing Multiple Myeloma
-Although multiple myeloma is often diagnosed based on tests, the patient’s symptoms and the doctor’s physical examination of the patient are also important. A diagnosis of multiple myeloma requires either:
1. A plasma cell tumor (proven by biopsy)
OR at least 10% of the cells in the bone marrow are plasma cells, AND at least one of the following:
-High blood calcium level Poor kidney function
-Low red blood cell counts (anemia)
-Holes in bones from tumor growth found on imaging studies
-An abnormal area in the bones or bone marrow on an MRI scan
-Increase in one type of light chains in the blood so that one type is 100 times more common than the other
OR
2. 60% or more plasma cells in the bone marrow
Smoldering myeloma
This term is used to mean early myeloma that is not causing any symptoms or problems. People with smoldering myeloma have some signs of multiple myeloma, such as any of the following Plasma cells in the bone marrow between 10 and 60% High level of monoclonal immunoglobulin (M protein) in the blood High level of light chains in the urine (also called Bence Jones protein) But they have normal blood counts, normal calcium levels, normal kidney function, no bone or organ damage, and no signs of amyloidosis. Smoldering myeloma often does not need to be treated right away. Light chain amyloidosis A diagnosis of light chain amyloidosis is made when the patient has both: Signs and symptoms of amyloidosis, and A biopsy that shows amyloid made up of light chains, PLUS any of the following: Elevated free light chains in the blood, Elevated light chains in the urine (also called Bence Jones protein), Abnormal plasma cells in the bone marrow

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Full details are in link below, but the jist is...
1) Mininum requirements: Inpatient unit, no contamination with HEPA filter allow allogenic(among diff. People) transplants, outpatient daycare unit, isolation rooms, dedicated stem cell laboratories, HLA testing lab, supportive services (radiotherapy, transfusion service, pharmacy, specialists)

2) Donors need INFORMED CONSENT (+risks told, can pull out anytime). Medical check ups to be done before the transplantation,. If incompatible, need a proper documentation of rationale, pregnancy test for child-bearing donors, a ton of lab tests to prevent contamination and ensure compatibility, CBC.

3)Team needs to be good in following out the procedures and being prepared in case of complications.

4) IMMUNOSUPPRESSIVE DRUGS.

5)For bone marrow transplant, the important thing is CONSENT

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Further info about transplantation in general

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Further info about transplantation in general