Abstract:
:The chemokine receptor CCR6 is expressed on naïve B cells, dendritic cell and T-cell subpopulations and is involved in cell navigation during organogenesis and recruitment in response to inflammatory stimuli. Gene-deficient C57BL/6 CCR6(-/-) mice infected with the protozoan parasite Leishmania (L.) major were able to mount a protective immune response and survived the infection. Whereas macrophage production of nitric oxide (NO), the key leishmanicidal effector molecule during the immune response to L. major, did not require CCR6, the migration of CD4(+) T cells to the site of infection was reduced in CCR6(-/-) mice. Furthermore, the induction of a T-cell-dependent delayed-type-hypersensitivity (DTH) reaction was defective in CCR6(-/-) mice, whereas resistance to re-infection was maintained in the absence of CCR6. We conclude that CCR6 contributes to the recruitment of T cells to the site of infection, but is largely dispensable for the control of L. major parasites during primary or secondary infection.
journal_name
Microbes Infectjournal_title
Microbes and infectionauthors
Lechner A,Ritter U,Varona R,Marquez G,Bogdan C,Körner Hdoi
10.1016/j.micinf.2006.12.002subject
Has Abstractpub_date
2007-03-01 00:00:00pages
291-9issue
3eissn
1286-4579issn
1769-714Xpii
S1286-4579(06)00415-1journal_volume
9pub_type
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