THE CONTEXT
CD4 T-cell subsets produce distinct cytokines that shape inflammation. Reciprocal interactions between lymphocytes and macrophages sustain chronic inflammatory reactions.
T-cell subsets and their cytokines
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Th1 cells produce IFN-g, which activates macrophages through the classical pathway.
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Th2 cells secrete IL-4, IL-5, and IL-13, which recruit and activate eosinophils and are responsible for alternative macrophage activation.
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Th17 cells produce IL-17 and other cytokines that induce chemokine secretion, recruiting mainly neutrophils.
Roles in defense and disease
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Th1 and Th17 cells participate in defense against many bacteria and viruses.
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Both subsets contribute to chronic inflammation in autoimmune diseases, including rheumatoid arthritis, psoriasis, and inflammatory bowel disease.
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Th2 cells contribute to defense against helminthic parasites and to allergic inflammation.
Reciprocal macrophage–T-cell activation
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Macrophages display antigens to T cells, express membrane costimulators, and produce cytokines such as IL-12 that stimulate T-cell responses.
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Activated T cells produce cytokines that recruit and activate macrophages, promoting further antigen presentation and cytokine secretion.
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This bidirectional cycle fuels and sustains chronic inflammation.
B lymphocytes and plasma cells
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Activated B lymphocytes and antibody-secreting plasma cells are often present at sites of chronic inflammation.
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Their antibodies may recognize persistent foreign antigens, self antigens, or altered tissue components at the inflammatory site.
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The specificity and importance of antibodies remain unclear in most chronic inflammatory disorders.