Cellular and humoral immune responses to mycobacterial heat shock protein‐65 and its human homologue in Takayasu's arteritis

• Published in: Clinical and experimental immunology Vol. 138; no. 3; pp. 547 - 553
• Main Authors: KUMAR CHAUHAN, S., KUMAR TRIPATHY, N., SINHA, N., SINGH, M., NITYANAND, S.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01-12-2004; Blackwell; Oxford University Press; Blackwell Science Inc
• Subjects: Adolescent; Adult; Antibodies - immunology; Antibody Formation - immunology; autoimmunity; Autoimmunity - immunology; Bacterial Proteins - immunology; Biological and medical sciences; CD4-Positive T-Lymphocytes - immunology; CD8-Positive T-Lymphocytes - immunology; Cell Division - immunology; Cells, Cultured; Chaperonin 60 - immunology; Chaperonins - immunology; Clinical Studies; Female; Fundamental and applied biological sciences. Psychology; Fundamental immunology; human HSP60; Humans; Immunity, Cellular - immunology; Immunoglobulin G - immunology; Immunoglobulin Isotypes - immunology; Immunopathology; Male; Medical sciences; Middle Aged; mycobacterial HSP65; T-Lymphocyte Subsets - immunology; Takayasu Arteritis - immunology; Takayasu's arteritis; Autoimmunity; Human; Immunopathology; Mycobacterium; Immune response; Cardiovascular disease; Homology; Cellular immunity; Vascular disease; Vasculitis; Immunology; Mycobacteriales; Systemic disease; Heat shock protein 65; Mycobacteriaceae; Heat shock protein 60; Bacteria; Actinomycetes; Takayasu's arteritis mycobacterial HSP65 human HSP60 autoimmunity; Takayashu arteritis
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1111/j.1365-2249.2004.02644.x

SUMMARY
Expression of heat shock protein (HSP)‐65 as well as infiltration of T‐cells in arterial lesions and raised levels of circulating antibodies against mycobacterial HSP65 (mHSP65) led us to the concept that mHSP65 or its human homologue (hHSP60) might be involved in the etiopathogenesis of Takayasu's arteritis (TA). Therefore, we investigated mHSP65 and hHSP60 reactive peripheral blood T‐cell subsets by BrdU incorporation assay and flow cytometry as well as investigating the different isotypes of anti‐mHSP65 and hHSP60 antibodies by ELISA. Eighty‐four percent (22/26) of the TA patients were observed to show T‐cell proliferation to mHSP65 and hHSP60 whereas only 16% (3/18) healthy controls showed such proliferation (P < 0·001). Both HSPs induced proliferation of exclusively CD4+ T‐cells and not CD8+ T‐cells. We also observed a significantly higher prevalence of only the IgG isotype reactive to mHSP65 and hHSP60 in TA as compared to HC (mHSP65: 92% TA versus 11% HC, P < 0·0001 and hHSP60: 84% versus 22%, P < 0·001). Our data show a significant correlation between mHSP65 and hHSP60 reactive T‐cells (CD3+: r = 0·901; CD4+: r = 0·968) as well as anti‐mHSP65 and anti‐hHSP60 IgG antibodies (r = 0·814) suggesting an infection induced autoimmunity in TA, possibly induced by molecular mimicry between mHSP65 and hHSP60 or other tissue specific antigens.