IgE cross-linking or lipopolysaccharide treatment induces recruitment of Th2 cells to the lung in the absence of specific antigen.
We previously showed that Th1 cells can increase recruitment of Th2 cells to the lungs even in the absence of the Th2-specific Ag. The fact that Th2 recruitment is independent from the Th2 cell Ag suggested that Th1 cells may support Th2 cell recruitment using their Ag-nonspecific proinflammatory functions. To investigate the potential for inflammatory stimuli that are distinct from Ag-specific signals to affect the recruitment of T cells, we tested whether cross-linking of IgE or treatment with LPS modulated influx of Th2 cells into the airways in the presence or absence of inhaled Ag. When naive mice that had been treated with OVA-specific Th2 cells and passively sensitized with anti-DNP IgE were challenged by intranasal administration of either DNP-haptenated OVA or DNP-BSA, increased numbers of Th2 cells were recruited to the lung compared with mice challenged intranasally with OVA alone. Intranasal administration of LPS also increased recruitment of Th2 cells to the airways. These two distinct inflammatory stimuli increased the numbers of recruited Th2 cells equally with or without concurrent challenge using the cognate Th2 Ag. This Ag-independent recruitment of Th2 cells to the lung was not associated with localization of these cells to the regional lymph nodes and was independent of Th2 cell activation. Interestingly, P- or E-selectin contributed to Th2 cell recruitment to the lung. These data suggest that Th2 cells of the adaptive immune response are similar to cells of the innate immune response in their lack of requirement for protein Ag to initiate cell recruitment. They demonstrate further that recruitment can occur independently of Ag-dependent activation.
Stephens
Robin
R
Division of Allergy and Immunology, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110.
Chaplin
David D
DD
D000276:Adjuvants, Immunologic / Q000008:administration & dosage; D000281:Administration, Intranasal; D000818:Animals; D000945:Antigens, Differentiation, T-Lymphocyte / Q000502:physiology; D002465:Cell Movement / Q000276:immunology*; D003432:Cross-Linking Reagents / Q000378:metabolism; D004140:Dinitrophenols / Q000008:administration & dosage; D004730:Endothelium, Vascular / Q000276:immunology / Q000378:metabolism; D018984:Epitopes, T-Lymphocyte / Q000502:physiology*; D005260:Female; D007073:Immunoglobulin E / Q000378:metabolism* / Q000502:physiology; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D008070:Lipopolysaccharides / Q000008:administration & dosage*; D008168:Lung / Q000166:cytology* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009093:Mucus / Q000378:metabolism; D017455:Receptors, IgE / Q000378:metabolism* / Q000502:physiology; D019087:Selectins / Q000502:physiology; D012710:Serum Albumin, Bovine / Q000008:administration & dosage; D018418:Th2 Cells / Q000166:cytology* / Q000276:immunology / Q000378:metabolism / Q000473:pathology
D000276:Adjuvants, Immunologic; D000945:Antigens, Differentiation, T-Lymphocyte; D003432:Cross-Linking Reagents; D004140:Dinitrophenols; D018984:Epitopes, T-Lymphocyte; D008070:Lipopolysaccharides; D017455:Receptors, IgE; D019087:Selectins; C034638:dinitrophenyl-bovine serum albumin; D012710:Serum Albumin, Bovine; D007073:Immunoglobulin E