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Interferon‐γ downregulates the proliferative response of hapten‐specific B cells stimulated by antigen and cytokines
Author(s) -
VOGEL LOTHAR,
PIKE BEVERLEY L.
Publication year - 1995
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.1995.8
Subject(s) - antigen , biology , immune system , hapten , interferon , immunology , b cell , cell growth , lymphokine , cytokine , t cell , microbiology and biotechnology , antibody , biochemistry
Summary IFN‐γ plays a role in many aspects of cellular interactions, both positive and negative. Among its functions during the immune response, the antagonistic effects of IFN‐γ and IL‐4 are well documented. Observations in our laboratory suggested that IFN‐γ could also interfere with the activation of single, antigen‐specific B cells by antigen and other cytokines. Closer examination revealed that IFN‐γ reduced the number of proliferating cell clones in response to antigen and a variety of cytokines, alone or in combination. Cell viability remained at the initial level and the cells were still able to produce Ig, albeit to a lesser extent than in the absence of IFN‐γ. On the other hand, the frequency of IgM secreting clones was not affected, whereas the total amount of secreted IgM was lower in the presence of IFN‐γ, probably due to the reduced cell number and a decrease in Ig production. In addition, proliferation was prevented when B cells were pre‐incubated with IFN‐γ and then stimulated by other cytokines. Kinetic studies revealed that INF‐γ had to be present from the onset of culture because delayed addition did not inhibit the proliferation of the B cells. After its initial action, IFN‐γ could be removed without abolishing the negative signal for proliferation. From these results it can be concluded that IFN‐γ transmits a signal that causes B cells to stop proliferating and prevents them from forming large clones.