Dynamics of antigen‐specific helper T cells at the initiation of airway eosinophilic inflammation

• Published in: European journal of immunology Vol. 31; no. 9; pp. 2669 - 2679
• Main Authors: Kaminuma, Osamu, Fujimura, Hisako, Fushimi, Keiko, Nakata, Aya, Sakai, Atsuko, Chishima, Susumu, Ogawa, Koji, Kikuchi, Matsuo, Kikkawa, Hideo, Akiyama, Kazuo, Mori, Akio
• Format: Journal Article
• Language: English
• Published: Weinheim WILEY‐VCH Verlag GmbH 01.09.2001
• Subjects: Adoptive Transfer; Airway; Animals; Asthma; Asthma - immunology; CD4 antigen; Cell Movement; Clone Cells; Eosinophil; Inflammation - immunology; intercellular adhesion molecule 1; Intercellular Adhesion Molecule-1 - physiology; Kinetics; Lung - immunology; Lung - ultrastructure; Lymphocyte Activation; Lymphoid Tissue - immunology; Male; Mice; Mice, Inbred BALB C; Migration; Ovalbumin - immunology; Pulmonary Eosinophilia - immunology; T helper cell; T-Lymphocytes, Helper-Inducer - immunology; T-Lymphocytes, Helper-Inducer - ultrastructure; Th2 Cells - immunology; Th2 Cells - transplantation; vascular cell adhesion molecule 1; Vascular Cell Adhesion Molecule-1 - physiology
• ISSN: 0014-2980; 1521-4141
• DOI: 10.1002/1521-4141(200109)31:9<2669::AID-IMMU2669>3.0.CO;2-Y

Bronchial asthma is characterized by chronic eosinophilic inflammation of the bronchial mucosa in which Th2 cells play crucial roles. Ovalbumin‐reactive Th2 clones were labeled with a fluorescent‐probe then infused into unprimed mice to elucidate the dynamics of antigen‐specific T cells involved in allergic inflammation. Infiltration of not only labeled antigen‐specific T cells, but alsounlabeled nonspecific CD4+ T cells into the bronchial mucosa following inhaled antigen challenge was detectable under confocal microscopy and flow cytometry. Accordingly, labeled T cells in the spleen were decreased, whereas those in hilar lymph nodes were increased upon antigen challenge. Approximately 45% of antigen‐specific T cells that migrated into the lungs bore CD25, while another early activation marker, CD69, was expressed on 80% of the migrated T cells. Accordingly, antigen challenge to the mice induced in situ proliferation of antigen‐specific T cells as well as bronchial epithelial cells in the lungs. Expression of vascular cell adhesion molecule (VCAM)‐1, but not intercellular adhesion molecule (ICAM)‐1, on the vascular endothelium in the lungs was enhanced following antigen challenge. Nevertheless, treatment with anti‐VCAM‐1 antibody, and also anti‐ICAM‐1 antibody strongly suppressed the accumulation of T cells, suggesting that both VCAM‐1 and ICAM‐1 are essential for antigen‐stimulated T cell mobilization into peripheral tissues. Our current study visualized the kinetics and the mechanism of antigen‐specific T cell migration in response to local challenge with a protein antigen.