The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.
Perforin-Dependent Brain-Infiltrating Cytotoxic CD8+ T Lymphocytes Mediate Experimental Cerebral Malaria Pathogenesis
Open accessAbstract
Experimental cerebral malaria (ECM) resulting from Plasmodium berghei ANKA infection involves T lymphocytes. However, the mechanisms of T cell-mediated pathogenesis remain unknown. We found that, in contrast to ECM-susceptible C57BL6 mice, perforin-deficient (PFP-KO) mice were resistant to ECM in the absence of brain lesions, whereas cytoadherence of parasitized erythrocytes and massive accumulation of activated/effector CD8 lymphocytes were observed in both groups of mice. ECM is induced in PFP-KO mice after adoptive transfer of cytotoxic CD8+ cells from infected C57BL6 mice, which were directed to the brain of PFP-KO mice. This specific recruitment might involve chemokine/chemokine receptors, since their expression was up-regulated on activated CD8 cells, and susceptibility to ECM was delayed in CCR5-KO mice. Thus, lymphocyte cytotoxicity and cell trafficking are key players in ECM pathogenesis.
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Cites
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Cited by
Immunological processes in malaria pathogenesis
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Brain microvessel cross‐presentation is a hallmark of experimental cerebral malaria
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Self-citation
Metadata
- Authors
- Nitcheu, J., Bonduelle, O., Combadiere, C., Tefit, M., Seilhean, D., Mazier, D., & Combadiere, B.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2003-02
- Volume
- 170
- Issue
- 4
- Pages
- 2221-2228
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1492482164
- Cited by
- 290
- References
- 35
- FWCI
- 10.55
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Nitcheu, J., Bonduelle, O., Combadiere, C., Tefit, M., Seilhean, D., Mazier, D., & Combadiere, B. (2003). Perforin-Dependent Brain-Infiltrating Cytotoxic CD8+ T Lymphocytes Mediate Experimental Cerebral Malaria Pathogenesis. The Journal of Immunology. https://doi.org/10.4049/jimmunol.170.4.2221
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