Transcription factors in allergic diseases

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Presentation transcript:

Transcription factors in allergic diseases David Préfontaine, MSc, Pierre-Olivier Fiset, PhD, Qutayba Hamid, MD, PhD Journal of Allergy and Clinical Immunology Volume 119, Issue 3, Pages 761-764 (March 2007) DOI: 10.1016/j.jaci.2006.11.015 Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 1 Immunocytochemistry for STAT6 was performed on bronchial biopsy specimens taken from a patient with atopic asthma (A) and from a healthy control subject (B). STAT6 expression was revealed in red by means of alkaline phosphatase–based immunocytochemistry. Journal of Allergy and Clinical Immunology 2007 119, 761-764DOI: (10.1016/j.jaci.2006.11.015) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 2 A, In situ hybridization was performed for GATA-3 mRNA by using 35S-labeled riboprobes in bronchial biopsy specimens from an atopic asthmatic subject. Dark-field illumination was used to visualize the brightly staining positive cells. B, Bronchoalveolar lavage fluid from atopic asthmatic subjects was probed with GATA-3 35S-labeled riboprobes (silver granule deposition from autoradiography) combined with IL-5 biotin-labeled riboprobes (brown staining from diaminobenzidine) to colocalize the 2 markers. The arrowhead points to an example of a GATA-3/IL-5 mRNA–positive cell. Journal of Allergy and Clinical Immunology 2007 119, 761-764DOI: (10.1016/j.jaci.2006.11.015) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 3 In situ hybridization for GATA-3 mRNA with 35S-labeled riboprobes in the nasal tissue explant. The biopsy specimens were obtained from an allergic subject and were cultured for 24 hours with ragweed allergen before processing. Journal of Allergy and Clinical Immunology 2007 119, 761-764DOI: (10.1016/j.jaci.2006.11.015) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 4 Sustained T-bet expression reduced GATA-3 mRNA levels, as measured by means of quantitative real-time PCR (A), and TH2 cytokine levels, as measured by means of ELISA and intracellular FACS staining (B). T-bet–transfected activated TH2 cells isolated from the skin of a patient with atopic dermatitis were either stimulated or unstimulated with anti-CD3 and anti-CD28 mAbs before quantitative PCR analysis. Cells were stimulated overnight before ELISA and 5 hours before FACS analysis. Notice the increased IFN-γ production in T-bet–transfected TH2 cells. Journal of Allergy and Clinical Immunology 2007 119, 761-764DOI: (10.1016/j.jaci.2006.11.015) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 5 In human subjects, FOXP3 deficiency causes immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome. Disease manifestations include eczema-like skin lesions (A) and inflammatory cell infiltration of the colon causing enteritis-like symptoms in a child (B; hematoxylin and eosin staining). A BALB/c Foxp3-deficient mouse displays gross abdominal pathology compared with that of its normal littermate (C): massive splenomegaly (long arrow), inflamed liver (short arrow), and engorged stomach (arrowhead) caused by inflamed stomach walls (ie, gastroparesis) are seen. Indeed, the spleen (D) displays intense periarteriolar infiltration by inflammatory cells (hematoxylin and eosin staining, original magnification ×400). Journal of Allergy and Clinical Immunology 2007 119, 761-764DOI: (10.1016/j.jaci.2006.11.015) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 6 A, Serum concentration of TH1 and TH2 cytokines in Foxp3-mutant mice relative to littermate control animals, as determined by using the Cytoplex Bead Array.8B, Levels of GATA-3 and T-bet transcripts in unfractionated splenocytes from wild-type and Foxp3-deficient littermate mice at ages 3, 9, and 17 days. Transcript levels were determined by means of real-time quantitative PCR, and results were normalized to hypoxanthine phosphoribosyl-transferase (HPRT) transcripts. Journal of Allergy and Clinical Immunology 2007 119, 761-764DOI: (10.1016/j.jaci.2006.11.015) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions