PMID- 12519308
OWN - NLM
STAT- MEDLINE
DCOM- 20030219
LR  - 20190513
IS  - 0019-2805 (Print)
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Linking)
VI  - 108
IP  - 1
DP  - 2003 Jan
TI  - gammadelta T cells contribute to the systemic immunoglobulin E response and local 
      B-cell reactivity in allergic eosinophilic airway inflammation.
PG  - 98-108
AB  - Allergic airway inflammation induced in mice is T-cell dependent and recruitment 
      of eosinophils to airspaces requires both alphabeta and gammadelta T cells. From 
      previous studies it is evident that alphabeta T cells are essential for the 
      allergic T helper type 2 (Th2)-like response, while the mechanistic contribution 
      of gammadelta T cells is still unclear. In this study, we have investigated the 
      role of gammadelta T cells in allergic airway eosinophilia induced by ovalbumin 
      hypersensitivity. By comparing the responsiveness to sensitizing allergen of 
      wild-type mice with that of T-cell receptor gammadelta knockout mice 
      (TCRgammadelta KO) we demonstrated that mice lacking gammadelta T cells are 
      defective in the systemic ovalbumin-specific immunoglobulin E (IgE) response. 
      Furthermore, after aerosol challenge with allergen, gammadelta T-cell deficient 
      mice exhibited a significantly decreased migration of B cells and natural killer 
      cells to airways and reduced levels of allergen-specific IgG and IgA in 
      bronchoalveolar lavage fluid. The role for B cells in the airway inflammation was 
      indicated by the impaired ability of mice lacking functional B cells to evoke an 
      eosinophilic response. The diminished eosinophilia in TCRgammadelta KO mice could 
      not be explained by a defective Th2 activation since these mice displayed a 
      normal IgG response in serum and an unaffected IG2b/IgG1 ratio in airways. 
      Analysis of immunoregulatory cytokines in isolated lung tissue, thoracic lymph 
      nodes and spleen further supported the notion that these mice are able to evoke a 
      sufficient activation of T helper cells and that gammadelta T cells are not 
      required for maintaining the Th2 profile. These results indicate that gammadelta 
      T cells contribute to allergic airway inflammation by pathways separate from 
      classical Th2 immune activation.
FAU - Svensson, Linda
AU  - Svensson L
AD  - Division of NBC Defence, Swedish Defence Research Agency, Umea, Sweden.
FAU - Lilliehook, Bo
AU  - Lilliehook B
FAU - Larsson, Roland
AU  - Larsson R
FAU - Bucht, Anders
AU  - Bucht A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (Cytokines)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Receptors, Antigen, T-Cell, alpha-beta)
RN  - 0 (Receptors, Antigen, T-Cell, gamma-delta)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Animals
MH  - B-Lymphocytes/*immunology
MH  - Bronchoalveolar Lavage Fluid/immunology
MH  - Cytokines/biosynthesis/genetics
MH  - Gene Expression
MH  - Immunoglobulin E/*biosynthesis
MH  - Immunoglobulin G/biosynthesis
MH  - Lung/immunology
MH  - Lymph Nodes/immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Pulmonary Eosinophilia/*immunology
MH  - Receptors, Antigen, T-Cell, alpha-beta/*analysis
MH  - Receptors, Antigen, T-Cell, gamma-delta/*analysis
MH  - Respiratory Hypersensitivity/*immunology
MH  - Spleen/immunology
MH  - T-Lymphocyte Subsets/*immunology
PMC - PMC1782860
EDAT- 2003/01/10 04:00
MHDA- 2003/02/20 04:00
PMCR- 2004/01/01
CRDT- 2003/01/10 04:00
PHST- 2003/01/10 04:00 [pubmed]
PHST- 2003/02/20 04:00 [medline]
PHST- 2003/01/10 04:00 [entrez]
PHST- 2004/01/01 00:00 [pmc-release]
AID - 1561 [pii]
AID - 10.1046/j.1365-2567.2003.01561.x [doi]
PST - ppublish
SO  - Immunology. 2003 Jan;108(1):98-108. doi: 10.1046/j.1365-2567.2003.01561.x.