Allergen-specific immunotherapy alters the expression of B and T lymphocyte attenuator, a co-inhibitory molecule, in allergic rhinitis

M. Okano, N. Otsuki, M. Azuma, T. Fujiwara, Shin Kariya, Y. Sugata, Takaya Higaki, K. Kino, Y. Tanimoto, K. Okubo, Kazunori Nishizaki

Research output: Contribution to journalArticle

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Abstract

Background: B7/CD28 family co-signalling molecules play a key role in regulating T cell activation and tolerance. Allergen-specific immunotherapy (SIT) alters allergen-specific T cell responses. However, the effect of SIT on the expression of various co-signalling molecules has not been clarified. Objective: We sought to determine whether SIT might affect the expression of three co-inhibitory molecules, programmed death (PD)-1, B7-H1 and B and T lymphocyte attenuator (BTLA), in Japanese cedar pollinosis (JCP). Methods: Peripheral blood mononuclear cells (PBMCs) were isolated from JCP patients who had or had not received SIT. PBMC were cultured in the presence or absence of Cry j 1, after which the cell surface expression of PD-1, B7-H1 and BTLA, as well as IL-5 production, were determined. In addition, the effect of BTLA cross-linking on IL-5 production was examined. Results: After Cry j 1 stimulation, no significant differences in PD-1 and B7-H1 expression were observed between SIT-treated and SIT-untreated patients. BTLA expression was down-regulated in untreated patients after Cry j 1 stimulation and up-regulated in SIT-treated patients. Up-regulation of BTLA in SIT-treated patients was particularly apparent in a CD4+ T cell subset. IL-5 production was clearly reduced among SIT-treated patients, and the observed changes in BTLA expression correlated negatively with IL-5 production. Moreover, immobilization of BTLA suppressed IL-5 production in JCP patients. Conclusion: These results suggest that both IL-5 production and down-regulation of BTLA in response to allergen are inhibited in SIT-treated patients with JCP. BTLA-mediated co-inhibition of IL-5 production may contribute to the regulation of allergen-specific T cell responses in patients receiving immunotherapy.

Original languageEnglish
Pages (from-to)1891-1900
Number of pages10
JournalClinical and Experimental Allergy
Volume38
Issue number12
DOIs
Publication statusPublished - Dec 2008

Fingerprint

Immunologic Desensitization
B-Lymphocytes
Immunotherapy
T-Lymphocytes
Interleukin-5
Cryptomeria
Seasonal Allergic Rhinitis
Allergens
Allergic Rhinitis
Blood Cells
T-Lymphocyte Subsets
Immobilization

Keywords

  • Allergen immunotherapy
  • Allergic rhinitis
  • BTLA
  • Cry j 1
  • IL-5

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Allergen-specific immunotherapy alters the expression of B and T lymphocyte attenuator, a co-inhibitory molecule, in allergic rhinitis. / Okano, M.; Otsuki, N.; Azuma, M.; Fujiwara, T.; Kariya, Shin; Sugata, Y.; Higaki, Takaya; Kino, K.; Tanimoto, Y.; Okubo, K.; Nishizaki, Kazunori.

In: Clinical and Experimental Allergy, Vol. 38, No. 12, 12.2008, p. 1891-1900.

Research output: Contribution to journalArticle

Okano, M. ; Otsuki, N. ; Azuma, M. ; Fujiwara, T. ; Kariya, Shin ; Sugata, Y. ; Higaki, Takaya ; Kino, K. ; Tanimoto, Y. ; Okubo, K. ; Nishizaki, Kazunori. / Allergen-specific immunotherapy alters the expression of B and T lymphocyte attenuator, a co-inhibitory molecule, in allergic rhinitis. In: Clinical and Experimental Allergy. 2008 ; Vol. 38, No. 12. pp. 1891-1900.
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AU - Okano, M.

AU - Otsuki, N.

AU - Azuma, M.

AU - Fujiwara, T.

AU - Kariya, Shin

AU - Sugata, Y.

AU - Higaki, Takaya

AU - Kino, K.

AU - Tanimoto, Y.

AU - Okubo, K.

AU - Nishizaki, Kazunori

PY - 2008/12

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N2 - Background: B7/CD28 family co-signalling molecules play a key role in regulating T cell activation and tolerance. Allergen-specific immunotherapy (SIT) alters allergen-specific T cell responses. However, the effect of SIT on the expression of various co-signalling molecules has not been clarified. Objective: We sought to determine whether SIT might affect the expression of three co-inhibitory molecules, programmed death (PD)-1, B7-H1 and B and T lymphocyte attenuator (BTLA), in Japanese cedar pollinosis (JCP). Methods: Peripheral blood mononuclear cells (PBMCs) were isolated from JCP patients who had or had not received SIT. PBMC were cultured in the presence or absence of Cry j 1, after which the cell surface expression of PD-1, B7-H1 and BTLA, as well as IL-5 production, were determined. In addition, the effect of BTLA cross-linking on IL-5 production was examined. Results: After Cry j 1 stimulation, no significant differences in PD-1 and B7-H1 expression were observed between SIT-treated and SIT-untreated patients. BTLA expression was down-regulated in untreated patients after Cry j 1 stimulation and up-regulated in SIT-treated patients. Up-regulation of BTLA in SIT-treated patients was particularly apparent in a CD4+ T cell subset. IL-5 production was clearly reduced among SIT-treated patients, and the observed changes in BTLA expression correlated negatively with IL-5 production. Moreover, immobilization of BTLA suppressed IL-5 production in JCP patients. Conclusion: These results suggest that both IL-5 production and down-regulation of BTLA in response to allergen are inhibited in SIT-treated patients with JCP. BTLA-mediated co-inhibition of IL-5 production may contribute to the regulation of allergen-specific T cell responses in patients receiving immunotherapy.

AB - Background: B7/CD28 family co-signalling molecules play a key role in regulating T cell activation and tolerance. Allergen-specific immunotherapy (SIT) alters allergen-specific T cell responses. However, the effect of SIT on the expression of various co-signalling molecules has not been clarified. Objective: We sought to determine whether SIT might affect the expression of three co-inhibitory molecules, programmed death (PD)-1, B7-H1 and B and T lymphocyte attenuator (BTLA), in Japanese cedar pollinosis (JCP). Methods: Peripheral blood mononuclear cells (PBMCs) were isolated from JCP patients who had or had not received SIT. PBMC were cultured in the presence or absence of Cry j 1, after which the cell surface expression of PD-1, B7-H1 and BTLA, as well as IL-5 production, were determined. In addition, the effect of BTLA cross-linking on IL-5 production was examined. Results: After Cry j 1 stimulation, no significant differences in PD-1 and B7-H1 expression were observed between SIT-treated and SIT-untreated patients. BTLA expression was down-regulated in untreated patients after Cry j 1 stimulation and up-regulated in SIT-treated patients. Up-regulation of BTLA in SIT-treated patients was particularly apparent in a CD4+ T cell subset. IL-5 production was clearly reduced among SIT-treated patients, and the observed changes in BTLA expression correlated negatively with IL-5 production. Moreover, immobilization of BTLA suppressed IL-5 production in JCP patients. Conclusion: These results suggest that both IL-5 production and down-regulation of BTLA in response to allergen are inhibited in SIT-treated patients with JCP. BTLA-mediated co-inhibition of IL-5 production may contribute to the regulation of allergen-specific T cell responses in patients receiving immunotherapy.

KW - Allergen immunotherapy

KW - Allergic rhinitis

KW - BTLA

KW - Cry j 1

KW - IL-5

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