title: ACP1 and Th class of immunological disease: evidence of interaction with gender.
abstract: BACKGROUND
  Data collected by our group in the past years indicate a relationship between ACP1 genetic polymorphism and susceptibility/resistance to immunological diseases. Recent observations suggest that through modulation of ZAP-70 activity, the enzyme may influence T cell activation. In view of the current interest in gender differences in autoimmune diseases we reviewed our data to enlighten possible effects of gender on the relationship between ACP1 and class of immunological disease.
  
  
  METHODS
  We studied three samples of subjects with allergic disorders of a total of 299 subjects, 71 subjects with Crohn's disease and 188 children with type 1 diabetes. Three-way contingency tables were analyzed by a log linear model and two-way contingency tables by chi(2) test.
  
  
  RESULTS
  There is an association between ACP1 and allergy (Th2 class) that depends on gender: the presence of the ACP1*A allele seems to make females more susceptible to allergic manifestations as compared to males. ACP1 is also associated with Crohn's disease and type 1 diabetes: the relationship between this class (Th1) of immunological diseases and ACP1 depends on gender. The presence of *A allele seems to make females less susceptible to this class of diseases as compared to males.
  
  
  CONCLUSIONS
  The ACP1*A allele which is associated with low ACP1 activity appears responsible for a complex relationship involving gender, ACP1 and Th1/Th2 orientation. Low ACP1 activity influencing ZAP-70 activity and in turn T cell activation seems to have opposite effects on Th1/Th2 orientation depending on gender.
authors.affiliation: Department of Biopathology and Imaging Diagnostics, University of Rome Tor Vergata, Rome, Italy. gloria@med.uniroma2.it
authors.forename: F
authors.initials: F
authors.lastname: Gloria-Bottini
authors.forename: N
authors.initials: N
authors.lastname: Bottini
authors.forename: G
authors.initials: G
authors.lastname: Renzetti
authors.forename: E
authors.initials: E
authors.lastname: Bottini
mesh_terms: D000328:Adult; D001327:Autoimmune Diseases / Q000235:genetics*; D002648:Child; D003424:Crohn Disease / Q000235:genetics / Q000276:immunology; D003922:Diabetes Mellitus, Type 1 / Q000235:genetics / Q000276:immunology; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D006967:Hypersensitivity / Q000235:genetics* / Q000276:immunology; D007223:Infant; D008297:Male; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D017027:Protein Tyrosine Phosphatases / Q000235:genetics*; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D012737:Sex Factors; D012882:Skin Tests; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology*
chemical_list: D011518:Proto-Oncogene Proteins; C490429:ACP1 protein, human; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D017027:Protein Tyrosine Phosphatases