title: Identical TCR beta-chain rearrangements in streptococcal angina and skin lesions of patients with psoriasis vulgaris.
abstract: Tonsillar infection with Streptococcus pyogenes may induce several nonsuppurative autoimmune sequelae. The precise pathogenetic mechanisms behind this clinically well-established association are still unresolved. Using TCR analysis, we sought to identify a link between streptococcal tonsillitis and the T cell-mediated autoimmune response in psoriasis. Three patients with streptococcal-induced psoriasis underwent tonsillectomy. Using size spectratyping and sequencing of TCR beta-chain variable region gene (TCRBV) rearrangements, we compared the TCR usage of psoriatic skin lesions, blood, tonsils, and tonsillar T cells fractionated according to the expression of the skin address in "cutaneous lymphocyte-associated Ag" (CLA). TCRBV-size spectratype analysis of the blood lymphocytes, tonsils, and the CLA-negative tonsillar T cells revealed largely unselected T cell populations. Instead, TCRBV gene families of the psoriatic lesions and skin-homing CLA-positive tonsillar T cells displayed highly restricted spectratypes. Sequencing of TCRBV cDNA identified various clonal TCRBV rearrangements within the psoriatic lesions that indicated Ag-driven T cell expansion. Several of these clonotypes were also detected within the tonsils and, in one of the patients, within the small subset of CLA-positive tonsillar T cells, suggesting that T cells from the same T cell clones were simultaneously present within skin and tonsillar tissue. Because after tonsillectomy psoriasis cleared in all three patients our observations indicate that T cells may connect psoriatic inflammation to streptococcal angina. They suggest that the chronic streptococcal immune stimulus within the tonsils could act as a source for pathogenic T cells in poststreptococcal disorders, and they may help to explain why eliminating this source with tonsillectomy may improve streptococcal-induced sequelae.
authors.affiliation: Department of Dermatology, Ludwig-Maximilians-University of Munich, Munich, Germany.
authors.forename: Laura
authors.initials: L
authors.lastname: Diluvio
authors.forename: Sigrid
authors.initials: S
authors.lastname: Vollmer
authors.forename: Petra
authors.initials: P
authors.lastname: Besgen
authors.forename: Joachim W
authors.initials: JW
authors.lastname: Ellwart
authors.forename: Sergio
authors.initials: S
authors.lastname: Chimenti
authors.forename: Joerg C
authors.initials: JC
authors.lastname: Prinz
mesh_terms: D000328:Adult; D000595:Amino Acid Sequence; D000945:Antigens, Differentiation, T-Lymphocyte; D000951:Antigens, Neoplasm / Q000235:genetics; D001483:Base Sequence; D002999:Clone Cells; D015333:Gene Rearrangement, beta-Chain T-Cell Antigen Receptor; D006801:Humans; D008562:Membrane Glycoproteins / Q000235:genetics; D008969:Molecular Sequence Data; D005810:Multigene Family; D014066:Palatine Tonsil / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D011565:Psoriasis / Q000276:immunology* / Q000473:pathology* / Q000601:surgery; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000096:biosynthesis* / Q000235:genetics / Q000302:isolation & purification*; D016201:Receptors, Lymphocyte Homing / Q000235:genetics; D012074:Remission Induction; D012214:Rheumatic Heart Disease / Q000276:immunology* / Q000473:pathology / Q000601:surgery; D012720:Severity of Illness Index; D013290:Streptococcal Infections / Q000276:immunology* / Q000473:pathology / Q000601:surgery; D013297:Streptococcus pyogenes / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D014068:Tonsillectomy; D014069:Tonsillitis / Q000276:immunology / Q000473:pathology / Q000601:surgery
chemical_list: D000945:Antigens, Differentiation, T-Lymphocyte; D000951:Antigens, Neoplasm; C063419:CTAGE1 protein, human; D008562:Membrane Glycoproteins; D016693:Receptors, Antigen, T-Cell, alpha-beta; D016201:Receptors, Lymphocyte Homing