Different T-bet expression patterns characterize particular reactive lymphoid tissue lesions.
OBJECTIVE
To investigate T-bet expression profiles in various lymphoid tissue diseases caused by intracellular pathogens and to compare them in disorders without an infective aetiology. Murine and in vitro experiments have shown that the expression/induction of T-bet, the master regulator of Th1 differentiation, can be achieved by obligate intracellular pathogens and high interferon (IFN)-gamma levels.


METHODS
Lymph node biopsies were analysed immunohistochemically employing single and double labelling for T-bet and CD20, CD4, CD8 and CD30 detection.


RESULTS
In disorders associated with high IFN-gamma levels and intracellular pathogens (infectious mononucleosis, HIV-associated lymphadenopathy, cat-scratch disease, and toxoplasmic lymphadenitis), T-bet-expressing CD4 cells were accompanied by significant numbers of T-bet-positive CD8 and B cells. A similar profile was also found in histiocytic necrotizing (Kikuchi) lymphadenitis, a disease of unknown cause. In contrast, T-bet expression in disorders without an infective aetiology was observed in only a small portion of lymphocytes.


CONCLUSIONS
Increased T-bet expression does not only identify intracellular infections in lymphoid tissue associated with high IFN-gamma levels, but also implies that, under these conditions, it becomes induced in B cells, which apparently support the Th1 response. T-bet expression in Kikuchi lymphadenitis underscores the hypothesis that it is caused by an intracellular microorganism.
Institute for Pathology, Charité, Campus Benjamin Franklin, Medical University Berlin, Germany.
K
K
Jöhrens
I
I
Anagnostopoulos
H
H
Dürkop
H
H
Stein
D018951:Antigens, CD20 / Q000032:analysis; D017252:CD3 Complex / Q000032:analysis; D015704:CD4 Antigens / Q000032:analysis; D016827:CD8 Antigens / Q000032:analysis; D005871:Castleman Disease / Q000378:metabolism / Q000473:pathology; D002372:Cat-Scratch Disease / Q000378:metabolism / Q000473:pathology; D015658:HIV Infections / Q000150:complications / Q000378:metabolism / Q000473:pathology; D020042:Histiocytic Necrotizing Lymphadenitis / Q000378:metabolism / Q000473:pathology; D006646:Histiocytosis, Langerhans-Cell / Q000378:metabolism / Q000473:pathology; D015618:Histiocytosis, Sinus / Q000378:metabolism / Q000473:pathology; D006801:Humans; D006965:Hyperplasia; D007150:Immunohistochemistry; D007244:Infectious Mononucleosis / Q000378:metabolism / Q000473:pathology; D017730:Ki-1 Antigen / Q000032:analysis; D008198:Lymph Nodes / Q000737:chemistry / Q000473:pathology; D008206:Lymphatic Diseases / Q000150:complications / Q000378:metabolism / Q000473:pathology; D008221:Lymphoid Tissue / Q000378:metabolism / Q000473:pathology*; D014066:Palatine Tonsil / Q000737:chemistry / Q000473:pathology; D012871:Skin Diseases / Q000150:complications / Q000378:metabolism / Q000473:pathology; D013154:Spleen / Q000737:chemistry / Q000473:pathology; D020825:T-Box Domain Proteins; D014123:Toxoplasmosis / Q000150:complications / Q000378:metabolism / Q000473:pathology; D014157:Transcription Factors / Q000096:biosynthesis*; D014376:Tuberculosis / Q000150:complications / Q000378:metabolism / Q000473:pathology; D000098815:T-bet Transcription Factor
D018951:Antigens, CD20; D017252:CD3 Complex; D015704:CD4 Antigens; D016827:CD8 Antigens; D017730:Ki-1 Antigen; D020825:T-Box Domain Proteins; D000098815:T-bet Transcription Factor; D014157:Transcription Factors