title: Mechanism of dinitrochlorobenzene-induced dermatitis in mice: role of specific antibodies in pathogenesis.
abstract: BACKGROUND
  Dinitrochlorobenzene-induced contact hypersensitivity is widely considered as a cell-mediated rather than antibody-mediated immune response. At present, very little is known about the role of antigen-specific antibodies and B cells in the development of dinitrochlorobenzene-induced hypersensitivity reactions, and this is the subject of the present investigation.
  
  
  RESULTS
  Data obtained from multiple lines of experiments unequivocally showed that the formation of dinitrochlorobenzene-specific Abs played an important role in the development of dinitrochlorobenzene-induced contact hypersensitivity. The appearance of dinitrochlorobenzene-induced skin dermatitis matched in timing the appearance of the circulating dinitrochlorobenzene-specific antibodies. Adoptive transfer of sera containing dinitrochlorobenzene-specific antibodies from dinitrochlorobenzene-treated mice elicited a much stronger hypersensitivity reaction than the adoptive transfer of lymphocytes from the same donors. Moreover, dinitrochlorobenzene-induced contact hypersensitivity was strongly suppressed in B cell-deficient mice with no DNCB-specific antibodies. It was also observed that treatment of animals with dinitrochlorobenzene polarized Th cells into Th2 differentiation by increasing the production of Th2 cytokines while decreasing the production of Th1 cytokines.
  
  
  CONCLUSIONS
  In striking contrast to the long-held belief that dinitrochlorobenzene-induced contact hypersensitivity is a cell-mediated immune response, the results of our present study demonstrated that the production of dinitrochlorobenzene-specific antibodies by activated B cells played an indispensible role in the pathogenesis of dinitrochlorobenzene-induced CHS. These findings may provide new possibilities in the treatment of human contact hypersensitivity conditions.
authors.affiliation: Department of Pharmacology, Toxicology and Therapeutics, School of Medicine, University of Kansas Medical Center, Kansas City, Kansas, United States of America.
authors.forename: Elizabeth Yan
authors.initials: EY
authors.lastname: Zhang
authors.forename: Aaron Yun
authors.initials: AY
authors.lastname: Chen
authors.forename: Bao Ting
authors.initials: BT
authors.lastname: Zhu
mesh_terms: D000818:Animals; D000906:Antibodies / Q000378:metabolism*; D001402:B-Lymphocytes / Q000187:drug effects; D002454:Cell Differentiation; D016207:Cytokines / Q000378:metabolism; D017449:Dermatitis, Allergic Contact / Q000473:pathology*; D004137:Dinitrochlorobenzene / Q000633:toxicity*; D005260:Female; D007111:Immunity, Cellular / Q000276:immunology; D007509:Irritants / Q000494:pharmacology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008813:Mice, Inbred ICR; D012867:Skin / Q000187:drug effects; D018417:Th1 Cells / Q000187:drug effects; D018418:Th2 Cells / Q000187:drug effects
chemical_list: D000906:Antibodies; D016207:Cytokines; D004137:Dinitrochlorobenzene; D007509:Irritants