Defective T-cell response to PHA and mitogenic monoclonal antibodies in male homosexuals with acquired immunodeficiency syndrome and itsin vitro correction by interleukin 2

1983 ◽  
Vol 3 (4) ◽  
pp. 332-340 ◽  
Author(s):  
Niculae Ciobanu ◽  
Karl Welte ◽  
Gerard Kruger ◽  
Salvatore Venuta ◽  
Jonathan Gold ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
T Cell ◽  
Acquired Immunodeficiency Syndrome ◽  
Cell Response ◽  
Interleukin 2 ◽  
T Cell Response ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome ◽  
Male Homosexuals

scholarly journals CD4 T cells in murine acquired immunodeficiency syndrome: polyclonal progression to anergy.

1992 ◽  
Vol 175 (6) ◽  
pp. 1589-1599 ◽  
Author(s):  
G Muralidhar ◽  
S Koch ◽  
M Haas ◽  
S L Swain
Keyword(s):  
T Cells ◽  
T Cell ◽  
Acquired Immunodeficiency Syndrome ◽  
Cd4 T Cells ◽  
Interleukin 2 ◽  
Cell Subset ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome ◽  
Phenotypic Shift ◽  
Kinetics Of

We have examined the kinetics of changes that occur in the helper T cell subset during murine acquired immunodeficiency syndrome, which occurs after infection with the mix of viruses known as BM5. We find that there is expansion of the CD4 T cells by 2 wk, 50% of the CD4 T cells become large as the disease progresses, and the CD4 T cell population is increasingly comprised of cells with a memory/activated phenotype. These effects are apparent by 2 wk postinfection, and the change is nearly complete by 6-8 wk. The phenotypic shift is paralleled by the loss of the ability of the CD4 T cells to proliferate or to produce interleukin 2 (IL-2), IL-3, IL-4, and interferon gamma in response to stimulation with mitogens, superantigen, or anti-CD3. There is no obvious expansion or deletion of CD4 T cells expressing particular V beta genes, as might be expected if a conventional superantigen were driving the changes. The results suggest, however, that the total CD4 population has been driven to anergy by some potent polyclonal stimulus directly associated with viral infection.

Intralymphatic Interleukin 2 Treatment in Patients with Acquired Immunodeficiency Syndrome: Preliminary Experience in Three Cases

Immunobiology ◽  
1986 ◽  
Vol 172 (3-5) ◽  
pp. 438-447 ◽  
Author(s):  
M. Gramatzki ◽  
H. Nüsslein ◽  
G.R. Burmester ◽  
W. Rüdl ◽  
N. Heyder ◽  
...  
Keyword(s):  
Acquired Immunodeficiency Syndrome ◽  
Interleukin 2 ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome

scholarly journals Mononucleosis and Antigen-Driven T Cell Responses Have Different Requirements for Interleukin-2 Signaling in Murine Gammaherpesvirus Infection

2010 ◽  
Vol 84 (20) ◽  
pp. 10923-10927 ◽  
Author(s):  
Michael Molloy ◽  
Weijun Zhang ◽  
Edward Usherwood
Keyword(s):  
T Cell ◽  
Cell Response ◽  
Interleukin 2 ◽  
T Cell Responses ◽  
T Cell Response ◽  
Long Term Memory ◽  
Murine Gammaherpesvirus ◽  
Cell Responses ◽  
Gammaherpesvirus 68 ◽  
Murine Gammaherpesvirus 68

ABSTRACT Interleukin-2 (IL-2) has been implicated as being necessary for the optimal formation of primary CD8+ T cell responses against various pathogens. Here we have examined the role that IL-2 signaling plays in several aspects of a CD8+ T cell response against murine gammaherpesvirus 68 (MHV-68). Exposure to MHV-68 causes a persistent infection, along with infectious mononucleosis, providing a model for studying these processes in mice. Our study indicates that CD25 is necessary for optimal expansion of the antigen-specific CD8+ T cell response but not for the long-term memory response. Contrastingly, IL-2 signaling through CD25 is absolutely required for CD8+ T cell mononucleosis.

Angiotropic (Intravascular) Large Cell Lymphoma of T-Cell Phenotype Presenting as Acute Appendicitis in a Patient With Acquired Immunodeficiency Syndrome

1999 ◽  
Vol 123 (4) ◽  
pp. 335-337 ◽  
Author(s):  
Denise M. Malicki ◽  
Yae K. Suh ◽  
Gregory N. Fuller ◽  
Sung S. Shin
Keyword(s):  
T Cell ◽  
Acute Appendicitis ◽  
Acquired Immunodeficiency Syndrome ◽  
Cell Lymphoma ◽  
Immunohistochemical Analysis ◽  
Large Cell ◽  
Cell Phenotype ◽  
Acquired Immunodeficiency ◽  
Large Cell Lymphoma ◽  
Immunodeficiency Syndrome

Abstract We describe a patient with acquired immunodeficiency syndrome who presented with acute appendicitis but was found to have angiotropic large cell lymphoma (ALCL) by pathologic examination of the appendectomy specimen, without acute inflammation. Very rare cases of angiotropic large cell lymphoma have been reported in patients with human immunodeficiency virus infection, and most cases of this rare lymphoma are of B-cell origin, but in this instance immunohistochemical analysis showed a T-cell phenotype.

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