Regulatory interactions between macrophages and T-cell subsets in Listeria monocytogenes-specific T-cell activation.

Abstract:

:Peritoneal exudate T lymphocytes from Listeria monocytogenes-immune mice in the presence of the homologous antigen (heat-killed L. monocytogenes) and normal macrophages showed L. monocytogenes-specific proliferative responses. Proliferation was inhibited by macrophages from L. monocytogenes- or Corynebacterium parvum-pretreated mice as well as by exogenous prostaglandin E(2). Macrophage-dependent inhibition of T-cell proliferation-at least in part-could be reversed by addition of indomethacin. When selected L. monocytogenes-immune Lyt T-cell subsets were cultured in the presence of inhibitory macrophages, pretreatment with anti-Lyt 1 antiserum plus complement completely abrogated proliferation and pretreatment with anti-Lyt 2 and anti-Lyt 3 antisera plus complement markedly reduced proliferation. However, a mixture (1:1) of the two preselected Lyt T-cell subsets resulted in complete reconstitution of proliferative responses. In contrast, when L. monocytogenes-immune peritoneal exudate T lymphocytes were treated with anti-Lyt antisera plus complement after culture, only treatment with anti-Lyt 1 antiserum plus complement affected proliferation, suggesting regulatory interactions between Lyt 1(+)23(-) and Lyt 1(-)23(+) T cells during in vitro culture which result in proliferation within the Lyt 1(+)23(-) T-cell subset. After rigorous depletion of residual macrophages and in the presence of indomethacin, pretreatment with anti-Lyt 1 antiserum plus complement, but not with anti-Lyt 2 and 3 antisera plus complement, eliminated proliferation. The data presented indicate that interactions between macrophages and Lyt T-cell subsets regulate L. monocytogenes-specific T-cell activation.

journal_name

Infect Immun

journal_title

Infection and immunity

authors

Kaufmann SH,Simon MM,Hahn H

doi

10.1128/IAI.38.3.907-913.1982

subject

Has Abstract

pub_date

1982-12-01 00:00:00

pages

907-13

issue

3

eissn

0019-9567

issn

1098-5522

journal_volume

38

pub_type

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