الفهرس Only 14 pages are availabe for public view
 |  | from | 161 |  |  |
| | | from | 161 | | |
Abstract
Background:Hypopigmented MF (HMF) is a variant of mycosis fungoides. Hypopigmented interface T-cell dyscrasia(TCD) is a distinct form of lymphoid dyscrasia that may progress to HMF. Aim of the work:To describe the predominant phenotype, T cell subsets, expression of TNF-Ü and granzyme B in both TCD and HMF and their changes following NB-UVB and upon development of repigmentation. Patients and methods:This prospective interventional study included 11 TCD and 9 HMF patients. They received NB-UVB sessions thrice weekly until complete repigmentation of a lesion or a maximum of 48 sessions. Pre-treatment and post-treatment biopsies were studied immunohistochemicallyusing anti CD4, CD8, CD45RA, CCR7, TNF-Ü and granzyme B antibodies. Results:Epidermal lymphocytes were CD8 predominant in 60% and 75% of TCD and HMF cases, respectively, while dermal lymphocytes were CD4 predominant in 60% and 62.5% of cases, respectively. The predominant epidermal subset was (CD45RA+, CCR7-)[64% of TCD and 50% of HMF cases]. On the other hand, the predominant dermal subset was (CD45RA-, CCR7-) [91% of TCD and 75% of HMF cases]. In both diseases, granzyme B was only expressed in the dermis, while TNF-Ü was expressed both in the epidermis and dermis. No significant difference existed between both diseases as regards number of sessions needed to achieve complete pigmentation or cumulative NB-UVB dose (p>0.05). NB-UVB significantly reduced epidermal CD4 and CD8 counts in both diseases (p{u2264}0.05)while dermal counts were not significantly changed (p>0.05).In both diseases, no significant difference existed as regards granzyme B or TNF-Ü expression after NB-UVB (p>0.05).Conclusion:Chronic antigen stimulation in both TCD and HMF leads to ultimate exhaustion of T cells which stands behind the indolent course of both diseases. Hypopigmentation in both diseases is mostly mediated by TNF-Ü and not granzyme-B. Repigmentation after NB-UVB in both diseases occurs independently from disappearance of dermal T cell infiltrate