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At least 235 records · Page 13Linked to original sources
PubMed1991

Progressive immune dysfunction in cats experimentally infected with feline immunodeficiency virus.

Within 6 months of infection with the Petaluma isolate of feline immunodeficiency virus, specific-pathogen-free domestic cats exhibited a decrease in the percentage and number of circulating CD4+ lymphocytes and in the CD4+/CD8+ T-cell ratio, along with a marginally significant depression of pokeweed mitogen-induced lymphocyte proliferation in vitro. There was no loss of responsiveness to concanavalin A during this stage, and the cats were capable of mounting a satisfactory antibody response to a T-dependent, synthetic polypeptide immunogen. The pokeweed mitogen response deficit became clearly demonstrable by 11 to 12 months postinfection. A decline in the lymphocyte proliferative response to concanavalin A and a diminished ability to mount an in vivo antibody response to the T-dependent immunogen evolved by 25 to 44 months postinfection. Virus infection did not affect the ability of cats to mount an antibody response to a T-independent synthetic polypeptide immunogen. These data indicate that feline immunodeficiency virus produces a slowly progressive deterioration of T-cell function but does not affect the ability of B cells to recognize and respond to a T-independent antigenic stimulus.

Amino Acid Sequence↗
PubMed1994

Lymphocytic choriomeningitis virus-induced immune dysfunction: induction of and recovery from T-cell anergy in acutely infected mice.

Acute infection of immunocompetent mice by lymphocytic choriomeningitis virus induces a potent cytotoxic T-lymphocyte response that eliminates infectious virus. Concurrently and paradoxically, there is a general suppression of lymphocyte responses to mitogens and to other infectious agents. Splenocytes from infected mice released significant amounts of gamma interferon in response to mitogenic stimulation in vitro, but neither interleukin 2 nor interleukin 4 was similarly elevated relative to the amounts released by control cells. Early T-cell receptor-proximal signaling events were found to be intact, confirming that the cells were viable and had received the mitogenic stimuli in an appropriate manner. Acutely infected adult thymectomized mice regained concanavalin A responsiveness in parallel with euthymic mice, if T cells were left unmanipulated for several weeks after clearance of virus from the mice. Therefore, although acute lymphocytic choriomeningitis virus infection has the effect of disrupting proliferation when the T-cell receptor is ligated, this state is only temporary. In contrast, T cells from persistently infected adult mice reveal long-lasting alterations in concanavalin A responsiveness.

Animals↗
PubMed1991

Immune dysfunction in mice with plasmacytomas. I. Evidence that transforming growth factor-beta contributes to the altered expression of activation receptors on host B lymphocytes.

Plasmacytoma-bearing mice (PC-mice) develop a polyclonal B cell immunodeficiency syndrome characterized by marked impairment of: a) primary antibody responses and b) proliferative responses to B cell mitogens. The present investigations used two-color flow cytometry to examine B lymphocytes from the spleens and lymph nodes of PC-mice and found decreased surface membrane expression of surface IgM (sIgM), transferrin receptors (TfR) and IgE FcR (CD23), increased expression of class II MHC, but normal expression of B220, Mel-14, Fc gamma RII, and Fc mu R. These changes were not related to the H chain class or the amount of Ig produced by the plasmacytoma. When cultured with IL-4, B lymphocytes from PC-mice increased their expression of sIgM and class II MHC, but not of CD23. Several findings implicate transforming growth factor-beta 1 (TGF-beta 1) in the mechanism that modulates receptor expression on B lymphocytes in PC-mice: a) ascites fluid from PC-mice contains large quantities of TGF-beta 1; b) supernatants of cultured spleen cells from PC mice contain up to eightfold more TGF-beta than is found with normal spleen cells; c) cloned plasmacytoma cells produce TGF-beta in vitro; and d) the abnormal phenotype of B cells from PC-mice, i.e., decreased CD23, sIgM, and TfR, and increased class II MHC, is induced on normal B cells cultured in the presence of TGF-beta 1. Because sIgM, TfR, class II MHC, and CD23 are molecules that play fundamental roles in the activation of normal B cells, their modulation by TGF-beta 1: a) identifies molecular mechanisms that could account for some of the known immunosuppressive properties of TGF-beta 1 and b) implicates TGF-beta in the pathogenesis of the polyclonal B cell immunodeficiency that is characteristic of plasma cell tumors.

Animals↗