چاپ صفحه |  صفحه نخست سامانه |  چکیده مقاله |  نویسندگان |  دانلود مقاله | دانشگاه علوم پزشکی تبریز |
| Cutaneous human papillomavirus (HPV) infection typically manifests with isolated papillomas. However, some patients in familial clustering develop extensive and protracted HPV infections, primarily the β-HPV types 5 and 8, with distinct cutaneous findings [1–3]; β-HPVs do not cause lesions in the general population. This clinical entity, epidermodysplasia verruciformis (EV), with autosomal recessive inheritance, is characterized by numerous cutaneous flat warts in childhood, which progress into verrucous tumors and evolve into squamous cell carcinomas later in life. The “typical” form of EV, not vulnerable to other infections, is caused by mutations in CIB1, TMC6, or TMC8, which impair keratinocyte-intrinsic immunity to β-HPV infection [3–5]. Mutations in other genes have been associated with “atypical” EV (Supplementary Table 1) [1–3]. Defects in those genes impair T-cell development or function, predisposing to β-HPV and other infections [1, 2]. We now describe an extended family with atypical EV in association with a mutation in an additional T-cell gene, ITK, encoding interleukin 2–inducible T-cell kinase (ITK). |
| نویسنده | نفر چندم مقاله |
|---|---|
| مهدی یوسفی | سوم |
| بهزاد منصوری | یازدهم |
| نام فایل | تاریخ درج فایل | اندازه فایل | دانلود |
|---|---|---|---|
| Inherited Interleukin .pdf | 1398/04/13 | 9519486 | دانلود |
