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The role of tumour necrosis factor-α in combination with interferon-γ or interleukin-1 in the induction of immunosuppressive macrophages because of <em>Mycobacterium avium</em> complex infection.
- Source :
-
Immunology . May96, Vol. 88 Issue 1, p61-67. 7p. - Publication Year :
- 1996
-
Abstract
- The role of some cytokines including tumour necrosis factor-α (TNF-α), interleukin-1α (IL-1α), interferon-γ (IFN-γ), transforming growth factor-β (TGF-β) and interleukin-6 (IL-6) in the generation of immunosuppressive macrophages (MΦs) in host spleen cells of Mycobacterium avium complex (MAC)-infected mice was studied. MΦ populations with potent suppressor activity against concanavalin A (Con A)-induced mitogenesis of splenocytes (SPCs) were elicited not only in euthymic but also in athymic nude mice during MAC infection. The suppressor MΦs are, therefore, inducible not only through a T-cell-dependent mechanism but also through T-cell-independent mechanism. However, MAC-induced MΦs of athymic mice displayed about four times lower suppressor activity than those of euthymic mice, indicating that mature T cells are important for MΦ activation to the highly immunosuppressive state. Anti-TNF, anti-IFN-γ, and anti-TGF-β antibodies (Abs) but not anti-IL-6 Ab inhibited in vivo generation of MAC-induced immunosuppressive MΦs, and the neutralizing efficacy was in the order of anti-IFN-γ Ab > antiTNF Ab > anti-TGF-β Ab. The effects of TNF-α, IL-1α, IL-6, and IFN-γ alone or combinations of them upon the acquisition of the suppressor activity by cultured splenic MΦs were studied. When normal splenic MΦs were treated with each cytokine for 3 days, TNF-α, IFN-γ, and IL-1α alone caused a slight elevation of their suppressive activity. Treatment of the normal MΦs with the combination of either TNF-α+IL-1α or TNF-α+IFN-γ yielded a marked increase in the suppressor activity, followed by IL-1α+IFN-γ. These findings indicate the important roles of TNF-α, IFN-γ, and IL-1α in the generation of MAC-induced suppressor MΦs. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00192805
- Volume :
- 88
- Issue :
- 1
- Database :
- Academic Search Index
- Journal :
- Immunology
- Publication Type :
- Academic Journal
- Accession number :
- 14079650
- Full Text :
- https://doi.org/10.1046/j.1365-2567.1996.d01-654.x