Inflammatory Thl Helper T Cell Responses

Phagocytic cells are capable of ingesting and destroying many different types of bacteria and parasites; however some pathogens have developed mechanisms for evading destruction once ingested. When infectious agents armed with these evasive strategies are encountered, small amounts of the pathogen are still degraded within phagolysomes and processed peptides are expressed on the surface of the phagocyte in association with MHC-II. When an inflammatory CD4+ helper T cell encounters the infected phagocyte, there is again nonspecific binding that allows the specific TcR and peptide/MHC-II complex to interact. This ligand and receptor interaction stimulates the Thl cell to release IL-2 that feedsback on the Thl cell causing proliferation and differentiation. The T cell progeny, armed inflammatory CD4+ T cells, now disperse to find target cells.

When the armed Thl cell encounters cells expressing the peptide/MHC-II complex, it is specific for the Thl cell it stimulated to release IFN-y, TNF-p, IL-2, IL-3, GM-CSF, MCF, and MIF. Interferon-y (IFN-y) activates the macrophage so it more effectively kills ingested bacteria. Tumor necrosis factor p (TNF-p) kills chronically infected macrophages that can no longer kill the bacteria, which releases the bacteria so fresh macrophages can engulf and destroy them. IL-2 causes further Th1 cell proliferation. Granulocyte-monocyte colony stimulating factor (GM-CSF) and interleukin-3 (IL-3) stimulate the production of more macrophages by the bone marrow. Macrophage chemotactic factor (MCF) and migration inhibition factor (MIF) cause macrophages to accumulate at the site of infection. Through these numerous effectors the Th1 cell of the adaptive immune system makes the cells of the innate system more effective and amplifies the immune response.

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