Immune responses of graft mesenteric lymph node in small bowel transplantation

Kanokogi, Hideki; Ko, Saiho; Kanehiro, Hiromichi; Hisanaga, Michiyoshi; Tatekawa, Yukihiro; Kanamura, Tetsuhiro; Okayama, Junji; Nakajima, Yoshiyuki

doi:10.1016/j.jss.2003.10.004

Cited by 4 publications

(1 citation statement)

References 30 publications

(18 reference statements)

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“…Our results show that the infiltration and activation of host cells in graft MLN clearly correlated with rejection severity. Similar results were reported by Kanokogi [23], who showed that donor lymphocytes in graft MLNs were rapidly replaced by host‐derived lymphocytes after transplantation, while our result showed less infiltration of host‐derived cells and higher persistence of donor cells in MR‐1‐treated ADAP−/− mice, which accounted for the observed beneficial effects.…”

Section: Discussionsupporting

confidence: 92%

ADAP deficiency combined with costimulation blockade synergistically protects intestinal allografts

Tian

Rodríguez-Barbosa

Pabst

et al. 2010

Transplant International

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Summary Adhesion and degranulation promoting adapter protein (ADAP) plays an important role in T cell activation. ADAP deficiency was recently found to prolong heart graft survival in mice. We investigated the role of ADAP in intestinal transplantation and the synergistic effect of ADAP deficiency and Costimulation blockade (CB). T cell proliferation and cytotoxic T lymphocyte (CTL) activity were determined. MHC mismatched intestinal allografts was transplanted heterotopically. Anti‐CD40L antibody was applied to the recipient. Upon stimulation with allogenic dendritic cells (DC), ADAP‐deficient (ADAP−/−) T cells displayed impaired proliferative responses compared with that of wild‐type (WT) T cells. In contrast, the CTL activity in ADAP−/− mice was comparable with that of WT mice. Rejection of intestinal allografts was ameliorated, but not prevented in ADAP−/− mice. Although CB alone was not sufficient to mitigate the rejection, the combination of CB and ADAP deficiency profoundly inhibited rejection. This was accompanied by less infiltration and activation of host lymphocytes in the gut‐associated lymphoid tissue of intestinal allografts. ADAP deficiency combined with CB protected the intestinal allografts synergistically. ADAP could be a novel target in the induction phase of the immune responses in organ transplantation.

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Section: Discussionsupporting

confidence: 92%