title: Immunoglobulin and CD8⁺ T-cell distribution in histologically distinctive tonsils of individuals with tonsillar focal infection.
abstract: CONCLUSIONS
  This study demonstrated that the common immunological mechanism, which involves aberration of immunoglobulin and T-cell distribution in histologically distinctive tonsils, may be associated with the pathogenesis of tonsillar focal infection.
  
  
  OBJECTIVE
  Tonsillar focal infection comprises a group of relatively common diseases combined with chronic tonsillar infection, is associated with unusual immune responses in tonsils, and may cause lesions in another distant target organ. This study aimed to investigate the distribution of inflammatory T cells and T-cell regulatory elements, such as programmed cell death-1 (PD-1) and Fork head box protein 3 (Foxp3), immunoglobulin production, and histological characteristics in tonsils from patients with tonsillar focal infection.
  
  
  METHODS
  Immunohistochemistry and reverse transcription-polymerase chain reaction (PCR) were used to compare the expression of CD8(+) T cells, immunoglobulins, and cytokines associated with immunoglobulin production in the tonsils of patients with IgA nephropathy (IgAN), palmoplantar pustulosis (PPP), rheumatoid arthritis (RA), and chronic tonsillitis.
  
  
  RESULTS
  The overexpression of CD8(+) T cells combined with decreased expression of Foxp3 and PD-1 and the aberration of immunoglobulin production, which may be due to the elevated expression of activation-induced deaminase (AID), B-cell-activating factor of the TNF family (BAFF), supporting isotype switching, and B-cell survival in the histologically distinctive tonsils.
authors: Department of Pathology, Harbin Medical University Cancer Hospital , Harbin , PR China.
authors: Hong-Xue
authors: HX
authors: Meng
authors: Rintaro
authors: R
authors: Ohe
authors: Hui-ning
authors: HN
authors: Li
authors: Su-ran
authors: SR
authors: Yang
authors: Takanobu
authors: T
authors: Kabasawa
authors: Tomoya
authors: T
authors: Kato
authors: Lei
authors: L
authors: Zhang
authors: Hiroya
authors: H
authors: Ohtake
authors: Akihiro
authors: A
authors: Ishida
authors: Nobuo
authors: N
authors: Ohta
authors: Xiao-ming
authors: XM
authors: Jin
authors: Seiji
authors: S
authors: Kakehata
authors: Mitsunori
authors: M
authors: Yamakawa
mesh_terms: D000328:Adult; D001172:Arthritis, Rheumatoid / Q000276:immunology* / Q000378:metabolism; D053264:B-Cell Activating Factor / Q000378:metabolism; D016827:CD8 Antigens / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000502:physiology*; D060833:Cellular Microenvironment; D003564:Cytidine Deaminase / Q000378:metabolism; D005260:Female; D005490:Focal Infection / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D051858:Forkhead Transcription Factors / Q000378:metabolism; D005922:Glomerulonephritis, IGA / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D007136:Immunoglobulins / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D014066:Palatine Tonsil / Q000473:pathology; D061026:Programmed Cell Death 1 Receptor / Q000378:metabolism; D011506:Proteins / Q000378:metabolism; D053668:Syndecan-1 / Q000378:metabolism; D014069:Tonsillitis / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D000098830:AICDA (Activation-Induced Cytidine Deaminase)
chemical_list: D053264:B-Cell Activating Factor; D016827:CD8 Antigens; C465580:FDCSP protein, human; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D007136:Immunoglobulins; C105992:PDCD1 protein, human; D061026:Programmed Cell Death 1 Receptor; D011506:Proteins; C508241:SDC1 protein, human; D053668:Syndecan-1; C505719:TNFSF13B protein, human; D000098830:AICDA (Activation-Induced Cytidine Deaminase); D003564:Cytidine Deaminase
keywords: Foxp3; IgA nephropathy; PD-1; chronic tonsillitis; palmoplantar pustulosis; rheumatoid arthritis