Role of anti-CD3 in modulation of Th1-type immune response in Shigella dysenteriae infection.
A murine model was used to evaluate the role of anti-CD3 in modulating a Th1-type response by restimulation of T-cells after immunization with the 57 kDa immunodominant antigen of Shigella dysenteriae 1 outer-membrane proteins (OMPs), followed by Shigella infection after immunization. To observe the effect of anti-CD3, other T-cell cultures were also established following anti-CD1, anti-IL2 and phytohaemagglutinin stimulation. Anti-CD3 stimulation of reconstituted T-cells showed 'mean' levels of CD4 and CD25 were enhanced by 34.5 and 31.1 % in immunized mice, which was comparable to 53.2 and 50.7 %, respectively, in challenged-immunized mice, and were dominant over CD8+ T-cells. Levels of IL2 generated by anti-CD3-stimulated T-cells of immunized mice were greater than those of unstimulated T-cells and were significantly elevated in challenged-immunized mice. The reactivity of T-cells indicated their complete responsiveness, as anti-CD3 antibody might not inhibit the migration of the macrophages but rather inhibit IL4. These macrophage factors synergistically act with anions towards an activated response, which in turn provokes IL2 secretion with a low degree of internalization of its receptor. Thus, sharing of IL2 to form a high-affinity receptor complex with CD4+ T-cells through motive signals suggested a generalized T-cell activation with increased humoral responses. Macrophage migration inhibition factor (MIF) and IL4 responses during anti-CD3 stimulation of immunized mice indicated that the role of anti-CD3 in generation of O2- is due to a synergistic effect by Th1 subsets of Th0 cells. The above findings should have implications for understanding the immunoregulatory role of anti-CD3 associated with 57 kDa antigen in immunoprophylactic measures.
Sinha
A K
AK
Division of Immunology and Vaccine Development, National Institute of Cholera & Enteric Diseases, Kolkata, India.
Bagchi
A K
AK
Division of Immunology and Vaccine Development, National Institute of Cholera & Enteric Diseases, Kolkata, India.
D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D000911:Antibodies, Monoclonal / Q000276:immunology; D000942:Antigens, Bacterial / Q000276:immunology; D018949:Antigens, CD1 / Q000276:immunology; D001425:Bacterial Outer Membrane Proteins / Q000276:immunology; D017252:CD3 Complex / Q000276:immunology*; D015704:CD4 Antigens / Q000032:analysis; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D004405:Dysentery, Bacillary / Q000276:immunology* / Q000382:microbiology; D005243:Feces / Q000382:microbiology; D006801:Humans; D016056:Immunodominant Epitopes / Q000276:immunology; D007074:Immunoglobulin G / Q000097:blood; D007376:Interleukin-2 / Q000032:analysis / Q000276:immunology; D015847:Interleukin-4 / Q000032:analysis; D019746:Intramolecular Oxidoreductases; D008213:Lymphocyte Activation; D008263:Macrophage Migration-Inhibitory Factors / Q000032:analysis; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D017382:Reactive Oxygen Species / Q000378:metabolism; D015375:Receptors, Interleukin-2 / Q000032:analysis; D012762:Shigella dysenteriae / Q000276:immunology* / Q000302:isolation & purification; D018417:Th1 Cells / Q000276:immunology*
D000907:Antibodies, Bacterial; D000911:Antibodies, Monoclonal; D000942:Antigens, Bacterial; D018949:Antigens, CD1; D001425:Bacterial Outer Membrane Proteins; D017252:CD3 Complex; D015704:CD4 Antigens; D016056:Immunodominant Epitopes; D007074:Immunoglobulin G; D007376:Interleukin-2; D008263:Macrophage Migration-Inhibitory Factors; D017382:Reactive Oxygen Species; D015375:Receptors, Interleukin-2; D015847:Interleukin-4; D019746:Intramolecular Oxidoreductases; C076231:Mif protein, mouse