Burn Injury Promotes Antigen-Driven Th2-Type Responses In Vivo

• Published in: The Journal of immunology (1950) Vol. 171; no. 8; pp. 3983 - 3990
• Main Authors: Guo, Zhijun, Kavanagh, Eamon, Zang, Yan, Dolan, Sinead M, Kriynovich, Sara J, Mannick, John A, Lederer, James A
• Format: Journal Article
• Language: English
• Published: United States Am Assoc Immnol 15-10-2003
• Subjects: Adoptive Transfer; Amino Acid Sequence; Animals; Antigens - administration & dosage; Antigens - immunology; Antigens - physiology; Burns - immunology; Burns - metabolism; CD4-Positive T-Lymphocytes - cytology; CD4-Positive T-Lymphocytes - immunology; CD4-Positive T-Lymphocytes - transplantation; Cell Differentiation - immunology; Cell Division - immunology; Cytokines - biosynthesis; Epitopes, T-Lymphocyte - immunology; Immunity, Innate; Male; Mice; Mice, Inbred BALB C; Mice, Transgenic; Molecular Sequence Data; Ovalbumin - administration & dosage; Ovalbumin - immunology; Ovalbumin - physiology; Peptide Fragments - administration & dosage; Peptide Fragments - immunology; Peptide Fragments - physiology; Th2 Cells - cytology; Th2 Cells - immunology; Th2 Cells - metabolism; Up-Regulation - immunology
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.171.8.3983

Severe injury induces detrimental changes in immune function, often leaving the host highly susceptible to developing life-threatening opportunistic infections. Advances in our understanding of how injury influences host immune responses suggest that injury causes a phenotypic imbalance in the regulation of Th1- and Th2-type immune responses. We report in this study, using a TCR transgenic CD4(+) T cell adoptive transfer approach, that injury skews T cell responses toward increased Th2-type reactivity in vivo without substantially limiting Ag-driven CD4(+) T cell expansion. The increased Th2-type response did not occur unless injured mice were immunized with specific Ag, suggesting that the phenotypic switch is Ag dependent. These findings establish that severe injury induces fundamental changes in the induction of Ag-specific CD4(+) Th cell responses favoring the development of Th2-type immune reactivity in vivo.