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Diagnosis

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Cytokines released by TH1 cells

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Why do we need interaction of Th1 and macrophage (macrophage activation)  at the first place?

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Why do we need interaction of Th1 and macrophage (macrophage activation)  at the first place?

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Some idea on why is macrophage activation is important :)

Source: Veterinary Immunology 9th edition in our class google drive

Yibi Tan

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https://docs.google.com/document/d/1MsDtQi7LaPoHY57xsI4_mWtOyC92yjPovvpLi-FOVao/edit?usp=sharing
Hey guys! This the google doc created for easier editing and finalizing our presentation content before the drawing, feel free to put in own's work and comment on other's too! :D

Yibi Tan

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Th1 cells produce cytokines which is interferon (IFN)-γ, interleukin (IL)-2, tumour-necrosis factor (TNF)-α and lymphotoxin) that are commonly associated with cell-mediated immune responses against intracellular pathogens, delayed-type hypersensitivity reactions, and induction of organ-specific autoimmune diseases.

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T cells with CD4 molecules bind peptides displayed on MHC II molecules. As discussed earlier, such peptides are derived from phagocytized sources, and thus these T cells interact with only with certain special, phagocytic cells. These cells are either macrophages or B cells.

Once a T cell recognizes its specific peptide antigen presented on a dendritic cell or B cell, the T cell becomes activated so that it now goes on to promote an aspect of an immune response. These activated T cells are called helper T cells, although this term does not accurately describe all of their functions.

Helper T cells develop in one of two directions, depending on the cytokine environment in which they are activated. These two types are called TH1 and TH2 cells.

The TH1 cells tend to form when there is lots of strong stimulation by the phagocytized antigen and lots of activation of the innate immune system. The TH2, by contrast, tend to form with weaker, more prolonged stimulation with less activation of innate mechanisms.

We have already discussed one important role that TH1 cells perform. This is to travel around the body to macrophages that have phagocytized the antigen. The TH1 cells bind to these cells and release IFN-gamma (interferon-gamma). In the macrophage, this cytokine increases the fusion of lysosomes with phagosomes, it especially cranks up mechanisms used to kill phagocytized microbes, and it attracts macrophages.

This activation of macrophages by IFN-gamma is important for dealing with sophisticated pathogens such as those that cause tuberculosis or leprosy. These pathogens can remain alive in macrophages after phagocytosis, and indeed, they really are intracellular parasites. They can live and reproduce inside unactivated macrophages for long periods.

Why aren't macrophages always "activated"? This probably is because the killing mechanisms of macrophages and neutrophils can damage the body as well as microbes. If activation of macrophages did not require a specific immune response, they might cause far more unnecessary damage to the body than they do. Consider that in tuberculosis the damage to the body is caused by macrophages fighting the bacteria rather than by anything the bacteria release.

A second role of helper T cells is to "help" B cells respond to antigens. Many antigens cannot by themselves cause a specific B cell to divide into a clone of antibody secreting plasma cells. In addition to binding the antigen, the B also phagocytizes some of the antigen and displays peptides on MHC II molecules. An activated helper T must bind to the cell and also release appropriate cytokines. Only when this happens, can the B cell divide into a clone.

The cytokines secreted are different for different types of helper T cells, which can be either TH1 or TH2. In the case of TH1, cells in the ensuing clone tend to undergo heavy chain switching so that they produce IgG, which is a good opsonin.

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A macrophage is a type of phagocyte, which is a cell responsible for detecting, engulfing and destroying pathogens and apoptotic cells. Macrophages are produced through the differentiation of monocytes, which turn into macrophages when they leave the blood. Macrophages also play a role in alerting the immune system to the presence of invaders.

CD4⁺T cells along with CD8⁺T cells make up the majority of T-lymphocytes. CD4⁺T cells after being activated and differentiated into distinct effector subtypes play a major role in mediating immune response through the secretion of specific cytokines. The CD4⁺T cells carry out multiple functions, ranging from activation of the cells of the innate immune system, B-lymphocytes, cytotoxic T cells, as well as nonimmune cells, and also play critical role in the suppression of immune reaction.

Type 1 T helper (Th1) cells produce interferon-gamma, interleukin (IL)-2, and tumour necrosis factor (TNF)-beta, which activate macrophages and are responsible for cell-mediated immunity and phagocyte-dependent protective responses. Th1 cells mainly develop following infections by intracellular bacteria and some viruses. Th1 cells are involved in the pathogenesis of organ-specific autoimmune disorders, Crohn's disease, Helicobacter pylori-induced peptic ulcer, acute kidney allograft rejection, and unexplained recurrent abortions.

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The mechanisms describing macrophage and CD4+ Th1 cells function and interaction

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Heng
i found this article and its quite relevant to the viral infection in macrophage. I am still reading on it and i guess you guys can have a look ?
http://jvi.asm.org/content/86/5/2826.full