Distinct genetic control of parasite elimination, dissemination, and disease after Leishmania major infection

0334105 - ÚMG 2010 RIV DE eng J - Článek v odborném periodiku
Kurey, Irina - Kobets, Tetyana - Havelková, Helena - Slapničková, Martina - Quan, L. - Trtková, Kateřina - Grekov, Igor - Svobodová, M. - Stassen, A. P. M. - Hutson, A. - Demant, P. - Lipoldová, Marie
Distinct genetic control of parasite elimination, dissemination, and disease after Leishmania major infection.
Immunogenetics. Roč. 61, č. 9 (2009), s. 619-633. ISSN 0093-7711. E-ISSN 1432-1211
Grant CEP: GA ČR GA310/06/1745; GA MŠMT(CZ) LC06009
Grant ostatní: EC(XE) 05-1000004-7761
Výzkumný záměr: CEZ:AV0Z50520514
Klíčová slova: Leishmania major * Parasite elimination * QTL mapping
Kód oboru RIV: EB - Genetika a molekulární biologie
Impakt faktor: 2.988, rok: 2009

Leishmania major infection in mice is an important model of host-pathogen relationship. Infected BALB/c mice exhibit high parasite numbers in lymph nodes and spleens and chronic disease with skin lesions, splenomegaly, hepatomegaly, increased serum IgE levels and cytokine imbalance. Linkage analysis integrated with study of multiple manifestations of infection in (BALB/c x CcS-11) F2 hybrids mapped 5 loci, 2 of which control parasite elimination or dissemination. Lmr5 influences parasite loads in spleens (+ skin lesions, splenomegaly, serum IgE, IL-4, and IFNg levels) and Lmr20 determines parasite numbers in draining lymph nodes (+ serum IgE and IFNg levels) but no skin or visceral pathology. Three additional loci do not affect parasite numbers but significantly influence disease phenotype - Lmr21: skin lesions, IFNg levels, Lmr22: IL-4 levels, Lmr23: IFNg levels, indicating that L. major-caused disease development includes critical regulations additional to control of parasite spread.
Trvalý link: http://hdl.handle.net/11104/0178927