Phagocytosis, antibody inhibition

Inhibition of inflammatory cytokines (Fig. 2) Humanized monoclonal anti-TNF antibodies (Infliximab (Remicade ), Adalimumab (Humira )) bind with high selectivity to human TNF-a and neutralize its activity. Thereby, infliximab decreases the effects of enhanced TNF levels during inflammatory disease such as production of proteases, chemokines, adhesion molecules, cyclooxygenase products (prostaglandins), and proinflammatory molecules such as interleukin-1 and -6. The antibodies may also recognize membrane-bound TNF-a on lymphocytes and other immune cells. These cells may subsequently become apoptotic or are eliminated via Fc-receptor-mediated phagocytosis. 

With long-term treatment, IgG subclass deficiencies can become marked (312). There is suppression of the antigen-antibody reaction, and since this reaction itself normally results in liberation of kinins, the latter is also suppressed. Failure of kinin liberation leads in turn to inhibition of invasion of sensitized leukocytes and reduced production and maturation of phagocytes. Undoubtedly, it is true that using minimal effective doses will avoid the most serious consequences, but the problem cannot be fully circumvented, since the antiinflammatory effects themselves involve some inhibition of the migration of leukocytes and phagocytosis. 

Chang, M.K. et al. Monoclonal antibodies against oxidized low-density lipoprotein bind to apoptotic cells and inhibit their phagocytosis by elicited macrophages evidence that oxidation-specific epitopes mediate macrophage recognition. Proc. Natl. Acad. Sci. USA 96 (1999) 6353-8. 

Inhibits cytokine production by activated T cells Decreases B cell proliferation Inhibits the actions of colony stimulating factors Slows antibody production Which one of the following agents increases phagocytosis by macrophages in patients with chronic granulomatous disease ... 

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