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Impact of MHC Class II Incompatibility on Localization of Mononuclear Cell Infiltrates to the Bronchiolar Compartment of Orthotopic Lung Allografts
Author(s) -
Nakashima Shinji,
Soong T. Rinda,
FoxTalbot Karen,
Qian Zhiping,
Rahimi Salma,
Wasowska Barbara A.,
Rohde Charles A.,
Chen Sabrina,
Garcia Joe G.N.,
Baldwin William M.
Publication year - 2005
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/j.1600-6143.2005.00782.x
Subject(s) - mhc class ii , mhc class i , immunology , antigen , major histocompatibility complex , medicine , pathology , antigen processing , cd74
Chronic pathological changes in transplanted lungs are unique because they center on the airways. We examined the relative role of MHC class I and II antigens in causing bronchial pathology in orthotopic lung transplants to rats maintained on cyclosporin A (CsA). Transplants mismatched for MHC class II antigens had significantly more peri‐bronchiolar infiltrates than MHC class I incompatible transplants. No significant increase in infiltrates was found in lung transplants incompatible for MHC class I plus II antigens compared to MHC class II antigens alone. Immunohistochemistry demonstrated that MHC class II antigen expression was confined to macrophages in MHC class I incompatible transplants, but was upregulated on bronchial epithelium in transplants with MHC class II incompatibilities. Vascular endothelium was notably devoid of MHC class II antigen expression in all transplants. However, both peri‐bronchial and peri‐vascular infiltrates were frequently cuffed by alveolar macrophages and type II pneumocytes that expressed MHC class II antigens. PCR analysis demonstrated that IFN‐γ and regulated on activation, normal T cells expressed and secreted (RANTES) were upregulated in MHC class II incompatible transplants. Thus, MHC class II incompatible orthotopic lung transplants in rats maintained on CsA immunosuppression undergo a bronchiolcentric upregulation of alloantigens.