Effects of Gamma‐Interferon and FK506 on Resting B Cell Proliferation of New Zealand Black/White F<sub>1</sub> Mice

Minoda, M; Ohno, Motoki; Tomioka, Yoshiki; Hamada, Kinya; Yamazoe, Yasushi; Higashikawa, Mitsuhiro; Sugishima, Hitoshi; Higashitani, Sumihiko; Funauchi, Masanori; Horiuchi, Atsushi

doi:10.1111/j.1348-0421.1992.tb02090.x

Cited by 7 publications

(2 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Alternatively, FK506 may also be able to influence B cell function directly. Our results are congruent with studies showing that FK506 inhibits in a dose-dependent manner B cell activation, B cell proliferation, and Ig production of resting B cells (Minoda et al, 1992;Sakuma et al, 2001;Schuller et al, 2004).…”

Section: Discussionsupporting

confidence: 92%

FK506 Controls CD40L-Induced Systemic Autoimmunity in Mice

Loser

Balkow

Higuchi

et al. 2006

Journal of Investigative Dermatology

View full text Add to dashboard Cite

Autoimmunity results from loss of mechanisms controlling self-reactivity. Autoimmune disorders play an increasingly important role and CD40-CD40 ligand (CD40L) interaction on immunocompentent cells is able to break established immunotolerance. To study the effects of the calcineurin-inhibitor FK506 on CD40L-induced systemic autoimmunity, CD40L transgenic (tg) mice, which spontaneously develop a mixed connective tissue-like disease, were treated with FK506 after onset of overt autoimmunity. Interestingly, FK506-treated CD40L tg mice showed significantly reduced autoimmune dermatitis scores and markedly decreased numbers of lesional infiltrating leukocytes. This finding was associated with diminished lymphadenopathy induced by FK506 treatment. Furthermore, FK506 suppressed the development of cytotoxic/autoreactive CD8(+) T cells as evidenced by the reduced expression of T cell activation markers in treated CD40L tg mice. Importantly, FK506 induced a significant reduction in autoantibody titers in the serum of CD40L tg animals. As CD40L tg mice develop nephritis leading to loss of renal function proteinuria was determined after FK506 injections. Notably, FK506 treatment re-established renal function as indicated by significantly reduced uric protein concentrations of treated CD40L tg mice. Together, these findings show the beneficial therapeutic effects of FK506 for the treatment of CD40L-induced autoimmunity. Additionally, these results demonstrate that FK506 is able to suppress ongoing severe autoimmune responses.

show abstract

Section: Discussionsupporting

confidence: 92%

FK506 Controls CD40L-Induced Systemic Autoimmunity in Mice

Loser

Balkow

Higuchi

et al. 2006

Journal of Investigative Dermatology

View full text Add to dashboard Cite

show abstract

“…Both induced immunoglobulin production by B cells, and the proliferation of stimulated B cells is inhibited, thus limiting the ability to respond to vaccine administration. Secondary antibody responses, natural killer or antibody‐dependent cytotoxic cell function are not inhibited ( 21–29).…”

Section: Immunosuppressive Effects Of Drugs Employed In Transplantationmentioning

confidence: 99%

The therapeutic prescription for the organ transplant recipient: the linkage of immunosuppression and antimicrobial strategies

Rubin

Ikonen

Gummert

et al. 1999

Transplant Infectious Dis

View full text Add to dashboard Cite

Infection and rejection, the two major barriers to successful organ transplantation, are closely linked, with immunosuppressive therapy being central to the pathogenesis of both. After almost two decades when azathioprine and prednisone, supplemented by antilymphocyte antibody therapy, were the cornerstones of post-transplant immunosuppressive programs, there has been a major increase in the therapeutic armamentarium available to treat rejection: cyclosporine, tacrolimus, mycophenolate mofetil, rapamycin, and antibodies directed against the interleukin-2 receptor. These agents are potent inhibitors of microbial specific T cell function, thus potentiating opportunistic infection with herpes group viruses, fungal and mycobacterial species, Strongyloides stercoralis, and a variety of intracellular pathogens. The mechanisms by which each of these drugs exerts its effects are an important determinant of the antimicrobial strategies that will be necessary to combat infection. Indeed, strategies to limit these infections are being linked to the nature of the immunosuppressive therapy required in a particular patient. Thus, the therapeutic prescription for the transplant patient is said to have two components: an immunosuppressive component to prevent and treat rejection, and an antimicrobial one to make it safe. In addition to using antimicrobial agents therapeutically, in the transplant patient prevention is stressed in which antibiotics are deployed prophylactically or preemptively.

show abstract