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Clearance of Chlamydia pneumoniae Infection in H‐2 Class I –/– Human Leucocyte Antigen‐A2.1 Monochain Transgenic Mice
Author(s) -
Tammiruusu A.,
Haveri A.,
Pascolo S.,
Lahesmaa R.,
Stevanovic S.,
Rammensee H.G.,
Sarvas M.,
Puolakkainen M.,
Vuola J. M.
Publication year - 2005
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2005.01645.x
Subject(s) - biology , antigen , cytotoxic t cell , ctl* , epitope , immunology , cd8 , immune system , major histocompatibility complex , chlamydia , human leukocyte antigen , virology , immunity , antibody , in vitro , genetics
CD8 + T cells have been suggested to play an important role in protective immunity against pulmonary Chlamydia pneumoniae infection in mice. Moreover, several classical major histocompatibility complex class I – restricted cytotoxic CD8 + T lymphocytes (CTL) specific for C. pneumoniae – derived peptides have been identified. Here, we studied the outcome of C. pneumoniae infection in human leucocyte antigen (HLA)‐A2.1 transgenic mice (HHD mice) that are only able to express a classical human class I molecule (HLA‐A2.1). C. pneumoniae infection was self‐restricted in HHD mice which were able to develop specific immune responses and a protective immunity against a subsequent rechallenge in a manner comparable to wildtype mice. Furthermore, accumulation of functional and C. pneumoniae‐ specific T cells to the site of infection was detected after challenge. Antigen processing and HLA‐A2.1‐dependent presentation was studied by immunizing the HHD mice with chlamydial outer protein N (CopN). Isolation of a peptide‐specific CTL line from the CopN‐immunized mice suggests that the HLA‐A2.1 molecule can support the development of CTL response against a chlamydial protein in mice. These findings suggest that the transgenic mouse model can be used for further characterization of the HLA‐A2.1‐restricted CD8 + T‐cell response during C. pneumoniae infection and for identification of CD8 epitopes from chlamydial antigens.

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