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Lymphokine regulation of surface Ia expression on rat B cells.

Abstract：

:Class II major histocompatibility antigens (Ia) play a major role in regulating T-B cell interactions; therefore, regulation of the amount of Ia on B cells may be an important point of control in the immune response. Mitogens in human and murine systems have been reported to increase Ia expression on B cells, and in the mouse the lymphokine BSF-1 (IL-4) markedly enhances Ia expression. This report describes studies of lymphokine and mitogen regulation of class II expression on rat B cells. Mitogens known to activate resting B cells, such as DxS/LPS, anti-IgM, STM, and Con A, induced increases in Ia expression. Highly purified murine IL-4 was found to have no Ia-enhancing activity on rat B cells, although the same preparation increased Ia expression eightfold on murine B cells. This confirms other recent reports that IL-4 is a species-specific lymphokine and will not cross even narrow phylogenetic barriers. Rat B cells were not refractory to lymphokine-induced enhancement of Ia expression, since lymphokine(s) contained in a Con A-induced supernatant enhanced Ia expression. Furthermore, murine IL-5-containing B151-CFS was able to markedly increase Ia expression on resting rat and mouse B cells. This activity was not lost after heat inactivation of B151-TRF2, indicating that B151-TRF1 (IL-5-like activity) was probably responsible for the increase in Ia expression. These results suggest Ia expression on rat B cells, like human and murine B cells, is an early activation event which is regulated by signals which act on resting B cells. Furthermore, while IL-4 is important in Ia regulation, it is not the only lymphokine involved, since the IL-4-free, B151-K12 supernatant was able to enhance Ia expression on resting rat and mouse B cells.

journal_name

Cell Immunol

journal_title

Cellular immunology

authors

Leitenberg D,Feldbush TL

doi

10.1016/0008-8749(88)90108-6

subject

Has Abstract

pub_date

1988-02-01 00:00:00

pages

451-60

issue

2

eissn

0008-8749

issn

1090-2163

pii

0008-8749(88)90108-6

journal_volume

111

pub_type

杂志文章

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