Faculty Research 1990 - 1999
Both immunity and hyperresponsiveness to Pneumocystis carinii result from transfer of CD4+ but not CD8+ T cells into severe combined immunodeficiency mice.
Document Type
Article
Publication Date
1992
Keywords
Antibodies-Fungal: bi, Antibody-Formation, Antigens-CD8: an, Immunity-Cellular, Immunization-Passive, Immunocompromised-Host, Mice, Mice-SCID, Pneumocystis-carinii: im, Pneumonia-Pneumocystis-carinii: im, pa, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S, T-Lymphocyte-Subsets: im, T4-Lymphocytes: im
First Page
673
Last Page
678
JAX Source
J Clin Invest 1992 Aug;90(2):673-8
Grant
AI25765, AI20232
Abstract
The opportunistic pathogen Pneumocystis carinii (Pc) is considered to be the leading cause of morbidity in patients with AIDS. It is important, therefore, to determine the immunological mechanisms of resistance to Pc. We have taken advantage of the lack of both T and B lymphocytes in severe combined immunodeficiency (scid) mice to determine the critical factors in resistance to spontaneously acquired Pc pneumonia. Using adoptive transfer of unfractionated or fractionated lymphocyte subsets or hyperimmune serum from congenic normal donors, we have demonstrated that effective immunity to Pc results from the action of CD4+ but not CD8+ T cells (in the absence of antibody) or from humoral immunity (in the absence of T cells). However, responses of CD4+ T cells (but not antibody) to already well-established burdens of Pc are often accompanied by a fatal hyperinflammatory reaction. The activity of CD4+ T cells against Pc thus illustrates a broadly applicable principle that T cell immunity represents a critical balance between consequences beneficial and harmful to the host.
Recommended Citation
Roths JB,
Sidman CL.
Both immunity and hyperresponsiveness to Pneumocystis carinii result from transfer of CD4+ but not CD8+ T cells into severe combined immunodeficiency mice. J Clin Invest 1992 Aug;90(2):673-8