Role of ICAM-1 (CD54) in the development of murine cerebral malaria

Favre, Nicolas; Laperousaz, Chen Da; Ryffel, Bernhard; Weiss, N.; Imhof, Beat A.; Rudin, W.; Lucas, Rudolf; Piguet, P F

doi:10.1016/s1286-4579(99)80513-9

Cited by 120 publications

(126 citation statements)

References 29 publications

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“…Dans ce contexte, il a été rapporté que l'histamine est essentielle au recrutement des lymphocytes T CD4 + et CD8 + spécifiques de l'antigène [29]. De nombreuses études ont démontré le rôle essentiel de la molécule d'adhésion ICAM-1 dans la séquestration des globules rouges infectés, et par conséquent dans le développement de la pathogenèse du paludisme, notamment par l'utilisation de souris déficientes en ICAM-1, qui sont résistantes au neuropaludisme [30,33] …”

Section: Rôle De L'histamine Dans La Pathogenèse Du Neuropaludismeunclassified

Rôle de l’histamine et des récepteurs histaminiques dans la pathogenèse du paludisme

et al. 2009

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Section: Rôle De L'histamine Dans La Pathogenèse Du Neuropaludismeunclassified

Rôle de l’histamine et des récepteurs histaminiques dans la pathogenèse du paludisme

et al. 2009

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“…CD40LϪ/Ϫ and CD54Ϫ/Ϫ mice, 6 isolated on the C57BL/6 background, were obtained from the Jackson Laboratory (Bar Harbor, ME). CD40Ϫ/Ϫ were obtained from R. Geha, Boston, MA.…”

Section: Micementioning

confidence: 99%

“…Briefly, 5-m sections were incubated overnight at room temperature with rat mAbs: anti-CD54 and anti-CD106 mAbs, as described previously, 6 or anti-CD40 mAb FGK45. 29 After washing, sections were incubated 1 hour with fluorescein isothiocyanate-labeled goat anti-rat IgG (Southern Biotechnology, Bioreba, Reinach, Switzerland).…”

Section: Immunohistochemistrymentioning

confidence: 99%

“…TNF is known to increase the expression of the adhesion molecules CD54 (ICAM-1) and CD106 (VCAM) on endothelia, 14 -16 which might contribute to increasing the adhesion of leukocytes and other cells and thereby disturbing the microcirculation in the brain and other organs. This pathogenic hypothesis is supported by the increased expression of CD54 and CD106 in the brain microcirculation during SM and the delayed mortality seen in mice treated with anti-CD11a mAb (LFA-1, a ␤2 integrin determinant) 6,17 or in CD54-deficient mice. 18 CD40 is a cell receptor belonging to the TNF receptor superfamily that can modulate cell proliferation, differentiation, and death.…”

mentioning

confidence: 92%

“…[3][4][5][6] In addition, there is a sequestration of macrophages, polymorphonuclear leukocytes (PMNs), parasitized red blood cells (pRBCs), and platelets in other organs, notably the lung. [5][6][7] Hence, because this syndrome is not limited to the brain, it is also referred as severe malaria (SM). Various studies using antibodies, recombinant cytokines, or knock-out mice have shown that the secretion of tumor necrosis factor (TNF) is an important effector of the mortality of SM.…”

mentioning

confidence: 99%

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Role of CD40-CD40L in Mouse Severe Malaria

Piguet

Kan

Vesin

et al. 2001

The American Journal of Pathology

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We explored the role of CD40-CD40L (CD154) in the severe malaria elicited by Plasmodium berghei anka infection in mice. Mortality was >90% by day 8 after infection in ؉/؉ mice, but markedly decreased in CD40؊/؊ or in CD40L؊/؊ mice, as well as in ؉/؉ mice treated with anti-CD40L monoclonal antibody. Parasitemia was similar in the different conditions. Breakdown of the blood-brain barrier was evident in infected ؉/؉, but not in CD40؊/؊ mice. Thrombocytopenia was less severe in CD40؊/؊ mice than in the ؉/؉ controls. Sequestration of macrophages in brain venules and alveolar capillaries was reduced in CD40؊/؊ or in CD40L؊/؊ mice, whereas sequestration of parasitized red blood cells or polymorphonuclear leukocytes in alveolar capillaries was CD40-CD40L-independent. CD40 mRNA was increased in the brain and lung of infected mice whereas CD40L was increased in the lung. Tumor necrosis factor plasma levels were similarly increased in infected ؉/؉ or CD40؊/؊ mice. Expression of CD54 and its mRNA levels in the brain were moderately decreased in CD40-deficient mice. Thus the mortality associated with severe malaria requires CD40-CD40L interaction that contributes to the breakdown of the blood-brain barrier, macrophage sequestration, and platelet consumption.

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CXCR3 determines strain susceptibility to murine cerebral malaria by mediating T lymphocyte migration toward IFN‐γ‐induced chemokines

et al. 2008

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Cerebral malaria (CM) results from the binding of infected erythrocytes and leukocytes to brain endothelia. The precise mechanisms underlying lymphocyte recruitment and activation in CM remain unclear. Therefore, the expression of various chemokines was quantified in brains of mice infected with Plasmodium berghei ANKA (PbA). Several chemokines attracting monocytes and activated T-lymphocytes were expressed at high levels. Their expression was almost completely abrogated in IFN-c ligand and receptor KO mice, indicating that IFN-c is an essential chemokine inducer in vivo. Surprisingly, the expression levels of chemokines, IFN-c and also adhesion molecules in the brain were not lower in CM-resistant Balb/c and DBA/2 mice compared to CM-sensitive C57BL/6 and DBA/1 mice, although T lymphocyte sequestration in the brain was significantly less in CMresistant than in CM-sensitive mice. This difference correlated with a higher up-regulation of the CXC chemokine receptor (CXCR)-3 on splenic T cells and a higher chemotactic response to IFN-c-inducible protein-10 (IP-10) in C57BL/6 compared to Balb/c mice. In conclusion, parasite-induced IFN-c in the brain results in high local expression levels of specific chemokines for monocytes and lymphocytes. The strain-dependent susceptibility to develop CM is more related to the expression of CXCR3 in circulating leukocytes than to the chemokine expression levels in the brain.

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Role of ICAM-1 (CD54) in the development of murine cerebral malaria

Cited by 120 publications

References 29 publications

Rôle de l’histamine et des récepteurs histaminiques dans la pathogenèse du paludisme

Rôle de l’histamine et des récepteurs histaminiques dans la pathogenèse du paludisme

Role of CD40-CD40L in Mouse Severe Malaria

CXCR3 determines strain susceptibility to murine cerebral malaria by mediating T lymphocyte migration toward IFN‐γ‐induced chemokines

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