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Major Classes of antibody
IgA, IgD, IgE, IgG, IgM
IgA- Protects the mucosal surfaces (nasal, tracheal)
IgD-
IgE- Mast cell, eosinophil degranulation (allergy or parasite)
IgG- becomes dominant a/b in circulation after acute infection, nuetralizes toxin
IgM- first a/b after infection (1st body defense?)

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Antibodies generally produced when there's an antigen present and B cell started to produce plasma cell to produce antibodies

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It binds to antigen and phagocytised by macrophage

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IgG, IgA, IgM, IgD, IgE

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Antibodies are mucoproteins that are found in the y-globulin fraction of serum on electrophoresis.

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just for reference if we gonna draw it out.

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ZAKIRAWARANIS Opsonization is the process by which a pathogen is marked and ingestion and eliminated by a phagocyte

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ZAKIRAWARANIS Opsonization is the process by which a pathogen is marked and ingestion and eliminated by a phagocyte

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Neutralisation is refers to the ability of specific antibodies to block the site on viruses that they use to enter their target cell

Complement is a system of plasma proteins that can be activated directly by pathogens or indirectly by pathogen-bound antibody, leading to a cascade of reactions that occurs on the surface of pathogens and generates active components with various effector functions

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IgG (The highest concentration class found in serum)
-Secreted by plasma cells in the spleen, lymph nodes and bone marrow. IgG binds to specific antigen on bacterial surfaces. This bind cause agglutination and lead to opsonization.

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MHC molecules bind with peptide fragments derived from pathogens and display them in the cell surface for recognition by T cells.
Why they do so ?
To  delete the pathogen

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it make it difficult for pathogens to evade immune responses in this way
1. polygenic-contain several loci encoding proteins of identical function.
2. polymorphism - ability to respond to the multitude and rapidly evolving pathogen

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The helper T cell binds to the antigen-MHC class II complex and is induced to release cytokines that induce the B cell to divide rapidly, making thousands of identical (clonal) cells. These daughter cells become either plasma cells or memory B cells.

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Difference between primary and secondary response

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Difference between primary and secondary response

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Primary immune response occurs when an antigen comes in contact to the immune system for the first time. During this time the immune system has to learn to recognize antigen and how to make antibody against it and eventually produce memory lymphocytes.

Secondary immune response occurs when the second time (3rd, 4th, etc.) the person is exposed to the same antigen. At this point immunological memory has been established and the immune system can start making antibodies immediately.

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Immune responses to antigens may be categorised as primary or secondary responses. The primary immune response of the body to antigen occurs on the first occasion it is encountered. Depending on the nature of the antigen and the site of entry this response can take up to 14 days to resolve and leads to the generation of memory cells with a high specificity for the inducing antigen. The humoral response, mediated by B cells with the help of T cells, produces high‐affinity and antigen‐specific antibodies. This is in contrast with the CD8 T‐cell response which leads to the generation of large numbers of antigen‐specific cells that are capable of directly killing infected cells. Antigen‐specific CD4 T cells, which provide help to B cells in the form of cytokines and other stimulatory factors, can also be expanded upon antigenic stimulation.The secondary response of both B‐ and T cells is observed following subsequent encounter with the same antigen and is more rapid leading to the activation of previously generated memory cells. This has some quantitative and qualitative differences from the primary response. 

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Immune responses to antigens may be categorised as primary or secondary responses. The primary immune response of the body to antigen occurs on the first occasion it is encountered. Depending on the nature of the antigen and the site of entry this response can take up to 14 days to resolve and leads to the generation of memory cells with a high specificity for the inducing antigen. The humoral response, mediated by B cells with the help of T cells, produces high‐affinity and antigen‐specific antibodies. This is in contrast with the CD8 T‐cell response which leads to the generation of large numbers of antigen‐specific cells that are capable of directly killing infected cells. Antigen‐specific CD4 T cells, which provide help to B cells in the form of cytokines and other stimulatory factors, can also be expanded upon antigenic stimulation.The secondary response of both B‐ and T cells is observed following subsequent encounter with the same antigen and is more rapid leading to the activation of previously generated memory cells. This has some quantitative and qualitative differences from the primary response. 

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IgE is the most important mediator of hypersensitivity or allergic reactions. When it binds to multivalent antigens there is activation of the mast cell, which releases chemical mediators stored in granules and capable of mediating local inﬂammatory reactions. This is called mast cell degranulation.

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IgE is the most important mediator of hypersensitivity or allergic reactions. When it binds to multivalent antigens there is activation of the mast cell, which releases chemical mediators stored in granules and capable of mediating local inﬂammatory reactions. This is called mast cell degranulation.

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Opsonization – Those microbes that replicate outside cells are removed by an interaction of the Fc part with speciﬁc receptors on the surface of elector cells. The antibodies coat the surface of the pathogen and allow binding of their Fc domains to Fc receptors present on elector cells. The macrophages and neutrophils then engulf the pathogen and internalize the microbe causing its destruction.

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Opsonization – Those microbes that replicate outside cells are removed by an interaction of the Fc part with speciﬁc receptors on the surface of elector cells. The antibodies coat the surface of the pathogen and allow binding of their Fc domains to Fc receptors present on elector cells. The macrophages and neutrophils then engulf the pathogen and internalize the microbe causing its destruction.