1. Primary cellular immunodeficiencies
Rebecca H. Buckley, MD 
Journal of Allergy and Clinical Immunology 
Volume 109, Issue 5, Pages (May 2002)
DOI: /mai
Copyright © 2002 Mosby, Inc. Terms and Conditions

2. Fig. 1
Locations of mutant proteins in activated CD4+ T cells identified in primary immunodeficiency diseases. Each mutant protein is identified by a red “X.” SLAM, Signaling lymphocyte activation molecule, SH2D1A, SLAM-associated protein; ATM, ataxia-telangiectasia mutation; NFAT, nuclear factor of activated T cells; WASP, Wiskott-Aldrich syndrome protein; β2m, β2-microglobulin; RFX, RFXAP, and CIITA, transcription factors. Used with permission from N Engl J Med. 2000;343:1317.
Journal of Allergy and Clinical Immunology  , DOI: ( /mai )
Copyright © 2002 Mosby, Inc. Terms and Conditions

3. Fig. 2
Relative frequencies of the different genetic types of SCID among 160 patients seen consecutively over 3 decades. RD, Reticular dysgenesis; CHH, cartilage hair hypoplasia.
Journal of Allergy and Clinical Immunology  , DOI: ( /mai )
Copyright © 2002 Mosby, Inc. Terms and Conditions

4. Fig. 3
Diagram showing that Jak3 is the major signal transducer for the common γc shared by multiple cytokine receptors. Mutations in the gene encoding Jak3 result in a form of autosomal recessive SCID that mimics SCID-X1 phenotypically.
Journal of Allergy and Clinical Immunology  , DOI: ( /mai )
Copyright © 2002 Mosby, Inc. Terms and Conditions

5. Fig. 4
Kaplan-Meier survival curve for 32 consecutive infants with SCID who received bone marrow transplants at Duke University Medical Center from HLA-identical (n = 2) or haploidentical (n = 30) donors before they were 3.5 months of age without pretransplantation chemoablation and without posttransplantation GVHD prophylaxis. Thirty-one (97%) infants survive for periods of 4 months to 20 years after transplantation. The 1 death occurred from a cytomegalovirus infection.
Journal of Allergy and Clinical Immunology  , DOI: ( /mai )
Copyright © 2002 Mosby, Inc. Terms and Conditions