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TAP-1 indirectly regulates CD4(+) T cell priming in Toxoplasma gondii infection by controlling NK cell IFN-gamma production

  1. Author:
    Goldszmid, R. S.
    Bafica, A.
    Jankovic, D.
    Feng, C. G.
    Caspar, P.
    Winkler-Pickett, R.
    Trinchieri, G.
    Sher, A.

  2. Author Address

    NIAID, Immunol Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. NCI, Canc & Inflammat Program, Canc Res Ctr, NIH, Frederick, MD 21702 USA. Univ Fed Santa Catarina, Dept Microbiol & Parasitol, Div Immunol, BR-88040900 Florianopolis, SC, Brazil.;Goldszmid, RS, NIAID, Immunol Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.;rgoldszmid@niaid.nih.gov
    1. Year: 2007
    2. Date: Oct
  2. Journal: Journal of Experimental Medicine
    1. 204
    2. 11
    3. Pages: 2591-2602
  4. Type of Article: Article
  5. ISSN: 0022-1007
  1. Abstract:

    To investigate if transporter associated with antigen processing (TAP)-1 is required for CD8(+) T cell-mediated control of Toxoplasma gondii in vivo, we compared the resistance of TAP-1(-/-), CD8(-/-), and wild-type (WT) mice to infection with the parasite. Unexpectedly, TAP-1(-/-) mice displayed greater susceptibility than CD8(-/-), beta(2)-microglobulin(-/-) (beta(2)m(-/-)), or WT mice to infection with an avirulent parasite strain. The decreased resistance of the TAP-1(-/-) mice correlated with a reduction in the frequency of activated (CD62L(low) CD44(hi)) and interferon (IFN)-gamma-producing CD4(+) T cells. Interestingly, infected TAP-1(-/-) mice also showed reduced numbers of IFN-gamma-producing natural killer (NK) cells relative to WT, CD8(-/-), or beta(2) m(-/-) mice, and after NK cell depletion both CD8(-/-) and WT mice succumbed to infection with the same kinetics as TAP-1(-/-) animals and displayed impaired CD4(+) T cell IFN-gamma responses. Moreover, adoptive transfer of NK cells obtained from IFN-gamma(-/-), but not IFN-gamma(-/-), animals restored the CD4(+) T cell response of infected TAP-1(-/-) mice to normal levels. These results reveal a role for TAP-1 in the induction of IFN-gamma-producing NK cells and demonstrate that NK cell licensing can influence host resistance to infection through its effect on cytokine production in addition to its role in cytotoxicity.

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  2. DOI: 10.1084/jem.20070634
  3. View record in Web of Science®
  4. WOS: 000250652200013

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