A specific defect in the proliferative capacity of B cells from old mice stimulated with autoreactive T cells

Prakash S. Nagarkatti; Aruna Seth; Mitzi Nagarkatti; Natarajan Muthusamy; Barbara Rychlik; Bondada Subbarao

doi:10.1016/0008-8749(89)90178-0

A specific defect in the proliferative capacity of B cells from old mice stimulated with autoreactive T cells

Prakash S. Nagarkatti, Aruna Seth, Mitzi Nagarkatti, Natarajan Muthusamy, Barbara Rychlik, Bondada Subbarao

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18 Scopus citations

Abstract

B lymphocytes from aged mice were found to be defective in their ability to proliferate in response to stimulation with an autoreactive T cell clone D1.4. The differentiative response leading to antibody secretion was also impaired in the auto D1.4 T cell-stimulated B cells from old mice in comparison to similarly stimulated B cells from young mice. The B cells from old mice were competent in activating the autoreactive T cells such that the T cells were induced to proliferate. The B cell defect appears to be restricted to a certain phase of B cell activation, since old mouse B cells responded to the auto D1.4 T cells by increasing cell surface Ia as well as size, but failed to incorporate tritiated thymidine. The responsiveness to interleukin-4 was found to be similar between B cells from young and old mice. It appeared that the B cells from old mice are specifically defective in progressing from the g₀ phase of cell cycle into the S phase when stimulated with the auto D1.4 T cells.

Original language	English
Pages (from-to)	102-113
Number of pages	12
Journal	Cellular Immunology
Volume	120
Issue number	1
DOIs	https://doi.org/10.1016/0008-8749(89)90178-0
State	Published - Apr 15 1989

Bibliographical note

Funding Information:
’ Supported in part by NIH Grants CA 45009 and CA45010 to P.S.N. and M.N., AI 21490, AG-05731, and an appropriation from the PSP funds of University of Kentucky to B.S. B.S. is a recipient of Research Career Development Award 1K 04AGOO422 from the NIH. ’ To whom all correspondence should be addresseda t The Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 405360230. 3 Abbreviations used: Ig, immunoglobulin; SMLR, syngeneic mixed lymphocyte reaction; IL, interleukin; ELISA, enzyme-linked immunosorbent assay.

Funding

’ Supported in part by NIH Grants CA 45009 and CA45010 to P.S.N. and M.N., AI 21490, AG-05731, and an appropriation from the PSP funds of University of Kentucky to B.S. B.S. is a recipient of Research Career Development Award 1K 04AGOO422 from the NIH. ’ To whom all correspondence should be addresseda t The Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 405360230. 3 Abbreviations used: Ig, immunoglobulin; SMLR, syngeneic mixed lymphocyte reaction; IL, interleukin; ELISA, enzyme-linked immunosorbent assay.

Funders	Funder number
National Institutes of Health (NIH)	CA 45009, CA45010, AG-05731
National Institute of Allergy and Infectious Diseases	R01AI021490
University of Kentucky	1K 04AGOO422

ASJC Scopus subject areas

Immunology

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title = "A specific defect in the proliferative capacity of B cells from old mice stimulated with autoreactive T cells",

abstract = "B lymphocytes from aged mice were found to be defective in their ability to proliferate in response to stimulation with an autoreactive T cell clone D1.4. The differentiative response leading to antibody secretion was also impaired in the auto D1.4 T cell-stimulated B cells from old mice in comparison to similarly stimulated B cells from young mice. The B cells from old mice were competent in activating the autoreactive T cells such that the T cells were induced to proliferate. The B cell defect appears to be restricted to a certain phase of B cell activation, since old mouse B cells responded to the auto D1.4 T cells by increasing cell surface Ia as well as size, but failed to incorporate tritiated thymidine. The responsiveness to interleukin-4 was found to be similar between B cells from young and old mice. It appeared that the B cells from old mice are specifically defective in progressing from the g0 phase of cell cycle into the S phase when stimulated with the auto D1.4 T cells.",

author = "Nagarkatti, \{Prakash S.\} and Aruna Seth and Mitzi Nagarkatti and Natarajan Muthusamy and Barbara Rychlik and Bondada Subbarao",

note = "Funding Information: {\textquoteright} Supported in part by NIH Grants CA 45009 and CA45010 to P.S.N. and M.N., AI 21490, AG-05731, and an appropriation from the PSP funds of University of Kentucky to B.S. B.S. is a recipient of Research Career Development Award 1K 04AGOO422 from the NIH. {\textquoteright} To whom all correspondence should be addresseda t The Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 405360230. 3 Abbreviations used: Ig, immunoglobulin; SMLR, syngeneic mixed lymphocyte reaction; IL, interleukin; ELISA, enzyme-linked immunosorbent assay.",

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AU - Rychlik, Barbara

AU - Subbarao, Bondada

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N2 - B lymphocytes from aged mice were found to be defective in their ability to proliferate in response to stimulation with an autoreactive T cell clone D1.4. The differentiative response leading to antibody secretion was also impaired in the auto D1.4 T cell-stimulated B cells from old mice in comparison to similarly stimulated B cells from young mice. The B cells from old mice were competent in activating the autoreactive T cells such that the T cells were induced to proliferate. The B cell defect appears to be restricted to a certain phase of B cell activation, since old mouse B cells responded to the auto D1.4 T cells by increasing cell surface Ia as well as size, but failed to incorporate tritiated thymidine. The responsiveness to interleukin-4 was found to be similar between B cells from young and old mice. It appeared that the B cells from old mice are specifically defective in progressing from the g0 phase of cell cycle into the S phase when stimulated with the auto D1.4 T cells.

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A specific defect in the proliferative capacity of B cells from old mice stimulated with autoreactive T cells

Abstract

Bibliographical note

Funding

ASJC Scopus subject areas

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