LFA-1-deficient mice show normal CTL responses to virus but fail to reject immunogenic tumor.

Schmits, Rudolf; Kündig, Thomas M.; Baker, D.; Shumaker, Grace; Simard, John; Duncan, Gordon S.; Wakeham, Andrew; Shahinian, Arda; Heiden, A. Van Der; Bachmann, Martin F.; Ohashi, Pamela S.; Mak, Tak W.; Hickstein, DD

doi:10.1084/jem.183.4.1415

Cited by 249 publications

(214 citation statements)

References 44 publications

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“…Similar results have been observed with antibodies against CD11a/ CD18 during thioglycollate peritonitis in mice [15] or rabbits [14], and during glycogen peritonitis in rabbits [13]. Mutant mice deficient in CD11a have decreased neutrophil emigration after 4 h of thioglycollate peritonitis [16]. Thus, studies in which CD11a is specifically inhibited or deficient suggest that CD11a/CD18 is critical to neutrophil emigration during acute peritonitis.…”

Section: Discussionsupporting

confidence: 71%

See 1 more Smart Citation

Combinatorial requirements for adhesion molecules in mediating neutrophil emigration during bacterial peritonitis in mice

Mizgerd

Quinlan

LeBlanc

et al. 1998

Journal of Leukocyte Biology

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To investigate the requirements for adhesion molecules in neutrophil emigration during peritonitis, mice received intraperitoneal injections of Streptococcus pneumoniae while the functions of multiple adhesion molecules were blocked. Emigration after 4 h was compromised by antibodies against ICAM-1 or genetic deficiency of ICAM-1. Anti-CD11a/CD18 antibodies decreased emigration in ICAM-1 mutant mice, suggesting that ICAM-1 independent emigration requires CD11/CD18 complexes. In contrast, mice mutant in ICAM-1 plus E-selectin showed no defect in emigration, suggesting that E-selectin commits neutrophils to an ICAM-1-dependent pathway during streptococcal peritonitis. However, in mutant mice lacking the three endothelial adhesion molecules E-selectin, P-selectin, and ICAM-1, emigration after 4 h was significantly compromised. Thus, P-selectin is essential to ICAM-1-and E-selectin-independent acute peritoneal inflammation. After 24 h of peritonitis, there were no differences between WT and E-selectin/P-selectin/ ICAM-1 mutant mice, demonstrating that these endothelial adhesion molecules are not essential to neutrophil emigration during later stages of peritonitis. J. Leukoc. Biol. 64: 291-297; 1998.

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Section: Discussionsupporting

confidence: 71%

“…CD11a/CD18 is critical to neutrophil emigration during peritonitis, as demonstrated by blocking antibody studies [13][14][15] and by CD11a deficiency [16]. CD11b/CD18 also binds ICAM-1 [17,18].…”

Section: Introductionmentioning

confidence: 99%

Combinatorial requirements for adhesion molecules in mediating neutrophil emigration during bacterial peritonitis in mice

Mizgerd

Quinlan

LeBlanc

et al. 1998

Journal of Leukocyte Biology

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“…We herein focus on the dissection of the CCR7-dependent immunological mechanisms in allograft rejection, by applying a model in which allogeneic tumor cells are readily rejected when installed as s.c. tumors [24][25][26][27]. Those tumor cells exhibit strong expression of MHC class I molecules, but not of MHC class II, which allowed us to focus on the role of CD8 + T cells in the process of growth control and rejection of MHC class Imismatched grafts [28].…”

Section: Discussionmentioning

confidence: 99%

The chemokine receptor CCR7 controls lymph node‐dependent cytotoxic T cell priming in alloimmune responses

Höpken

Droese

et al. 2004

Eur J Immunol

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The chemokine receptor CCR7 and its ligands regulate migration and colocalization of T cells and mature dendritic cells to and within secondary lymphoid organs. The requirement of CCR7 in efficient priming of allospecific cytotoxic CD8 + T cells is poorly characterized. Here, we demonstrate a role for CCR7 in the initiation of an alloimmune response and in the development of transplant rejection. Remarkably, in a model of acute allogeneic tumor rejection, CCR7 -/-mice completely failed to reject subcutaneously injected MHC class I mismatched tumor cells and cytotoxic activity of allospecific T cells was severely compromised. When solid tumors derived from wild-type mice were transplanted, recipient CCR7 -/-mice were capable of rejecting the allografts. In contrast, tumor allografts transplanted from CCR7 -/-donors onto CCR7 -/-recipients showed allograft survival up to 28 days, suggesting a critical function of CCR7 on donor-type passenger leukocytes in the initiation of cytotoxic CD8 + T cell responses. In a heterotopic heart transplantation model CCR7 deficiency resulted in significantly prolonged but not indefinite allograft survival. Additional prolongation of graft survival was observed when hearts from CCR7 -/-mice were used as donor organs. Our results define a key role for CCR7 in allogeneic T cell priming within the context of draining lymph nodes.

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“…CBA × C57BL/6, C57BL/6 and LFA-1 -/-mice were bred in the animal facilities at the Karolinska Institute. Breeding pairs of LFA-1 -/-mice [23] were kindly provided by Dr Tak W. Mak. B cells from individual spleens of their offspring were tested, as the mice were outbred.…”

Section: Methodsmentioning

confidence: 99%

Assessment of the Role of Leucocyte Function‐Associated Antigen‐1 in Homotypic Adhesion of Activated B Lymphocytes

1998

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Greicius G, Tamosiunas V, Severinson E. Assessment of the Role of Leucocyte Function-Associated Antigen-1 in Homotypic Adhesion of Activated B Lymphocytes. Scand J Immunol 1998;48:642-650 In this study we investigated how T-cell-dependent stimuli, via interleukin-4 (IL-4) or CD40 ligation, influence homotypic B-cell adhesion when compared with induction by the T-cell-independent stimulus lipopolysaccharide (LPS). Using primary murine B cells, we found that T-cell-dependent stimulation led to increased aggregation as compared to that induced by LPS. The adhesion was to a large extent dependent on the adhesion molecule, lymphocyte function-associated antigen-1 (LFA-1). We found that activation of B cells with the mitogenic stimuli induced an increased avidity of LFA-1 for its ligand, intercellular adhesion molecule-1 (ICAM-1). The increase was stable and different from that induced by phorbol esters. Although adhesion was reduced using B cells from LFA-1 -/-mice, aggregation occurred in response to T-celldependent stimuli. Our data suggest that adhesion of B lymphocytes is regulated in different modes. One is induced by antigen and leads to a transient conformational change of the LFA-1 molecule. Another is induced by mitogenic stimuli and leads to stable avidity increase of LFA-1, possibly via activation of cytoskeletal anchorage. A third is LFA-1 independent, of low avidity and is induced by T-cell-dependent stimuli.

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LFA-1-deficient mice show normal CTL responses to virus but fail to reject immunogenic tumor.

Cited by 249 publications

References 44 publications

Combinatorial requirements for adhesion molecules in mediating neutrophil emigration during bacterial peritonitis in mice

Combinatorial requirements for adhesion molecules in mediating neutrophil emigration during bacterial peritonitis in mice

The chemokine receptor CCR7 controls lymph node‐dependent cytotoxic T cell priming in alloimmune responses

Assessment of the Role of Leucocyte Function‐Associated Antigen‐1 in Homotypic Adhesion of Activated B Lymphocytes

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