Activated and cycling lymphocytes in benign dermal lymphocytic infiltrates including psoriatic skin lesions

1985 ◽  
Vol 278 (2) ◽  
pp. 92-96 ◽  
Author(s):  
G. Lange Wantzin ◽  
J. K. Larsen ◽  
I. J. Christensen ◽  
E. Ralfkiaer ◽  
M. Tjalve ◽  
...  
2016 ◽  
Vol 44 (7) ◽  
pp. 845-846 ◽  
Author(s):  
Ikuko Ueda-Hayakawa ◽  
Chuyen Nguyen Thi Hong ◽  
Yoko Ueki ◽  
Naotomo Kambe ◽  
Hiroyuki Okamoto

2010 ◽  
pp. 3603-3616 ◽  
Author(s):  
J. Braun ◽  
J. Sieper

The spondyloarthritides are a group of inflammatory rheumatic diseases with predominant involvement of axial and peripheral joints and entheses, together with other characteristic clinical features, including inflammatory back pain, sacroiliitis, peripheral arthritis (mainly in the legs), enthesitis, dactylitis, preceding infection of the urogenital/gastrointestinal tract, psoriatic skin lesions, Crohn-like gut lesions, anterior uveitis, and a family history of Spondyloarthritis. They are the second most frequent inflammatory rheumatic diseases after rheumatoid arthritis....


2020 ◽  
Vol 21 (15) ◽  
pp. 5363
Author(s):  
Agnieszka Gęgotek ◽  
Pedro Domingues ◽  
Adam Wroński ◽  
Elżbieta Skrzydlewska

The dermal fibroblasts are in constant contact with the cells of the immune system and skin epidermis. Therefore, they are essential for the development of lesions in psoriasis. The aim of this study was to assess the changes in the proteomic profile of fibroblasts in the dermis of psoriasis patients, and to discuss the most significant changes and their potential consequences. The proteomic results indicate that fibroblast dysfunction arises from the upregulation of proinflammatory factors and antioxidant proteins, as well as those involved in signal transduction and participating in proteolytic processes. Moreover, downregulated proteins in psoriatic fibroblasts are mainly responsible for the transcription/translation processes, glycolysis/ adenosine triphosphate synthesis and structural molecules. These changes can directly affect intercellular signaling and promote the hyperproliferation of epidermal cells. A better understanding of the metabolic effects of the proteomic changes observed could guide the development of new pharmacotherapies for psoriasis.


2001 ◽  
Vol 116 (5) ◽  
pp. 721-727 ◽  
Author(s):  
Khusru Asadullah ◽  
Markus Friedrich ◽  
Sandra Hanneken ◽  
Christoph Rohrbach ◽  
Heike Audring ◽  
...  

2015 ◽  
Vol 37 (2) ◽  
pp. 359-368 ◽  
Author(s):  
HAI-YAN JIA ◽  
YING SHI ◽  
LONG-FEI LUO ◽  
GUAN JIANG ◽  
QIONG ZHOU ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-13
Author(s):  
Piotr Kupczyk ◽  
Adam Reich ◽  
Mariusz Gajda ◽  
Marcin Hołysz ◽  
Edyta Wysokińska ◽  
...  

Psoriasis is an immunogenetic skin disease manifesting as plaque lesions on the skin. Patients with psoriasis frequently suffer from itch, an unpleasant sensation causing a desire to scratch. Psoriatic itch is mainly transmitted by unmyelinated C-fibers; however, the exact molecular mechanism of psoriatic itch is still unexplained. Protein gene product 9.5 (PGP 9.5) is a panneurological marker commonly used for analysis of peripheral peptidergic and nonpeptidergic nerves and identification of cutaneous neuro-immune-endocrine cells. However, some studies suggested that nonneuronal cells, like keratinocytes, may also express PGP 9.5. This phenomenon might be linked with impaired axonal transport, keratinocyte injury, or dysfunctions of neuro-immune-cutaneous connections. The aim of this study was to analyze the expression of PGP 9.5 in psoriatic skin. We observed significantly altered density of PGP 9.5-positive axonal nerve terminals in pruritic lesional (p=0.04) and nonlesional psoriatic skin (p>0.001) compared with controls. In contrast, no significant differences were observed between psoriatic skin without itch and controls. Furthermore, PGP 9.5 expression by suprabasal keratinocytes (SBKs) was significantly increased in itchy skin lesions (p=0.007) compared to skin without itch, and a positive correlation was observed between PGP 9.5 expression and itch intensity (r=0.64; p=0.02). Our findings indicate changes in peripheral innervations and psoriatic keratinocytes, which may influence neuro-immune-cutaneous homeostasis and modulate itch transmission.


2008 ◽  
Vol 37 (2) ◽  
pp. 63-71 ◽  
Author(s):  
G. F. Sudha ◽  
M. Santosh Kumar ◽  
V. Swetha ◽  
N. Gobinath

2017 ◽  
Vol 9 (2) ◽  
pp. 26-29 ◽  
Author(s):  
Yuki Matsuura-Otsuki ◽  
Takaaki Hanafusa ◽  
Hiroo Yokozeki ◽  
Kyoko Watanabe

A 42-year-old Japanese man presented with persistent headache during treatment for psoriatic arthritis (PsA) with infliximab. Treatment with infliximab was initiated 3 years before and the psoriatic skin lesions with arthritis were well controlled. However, after 21 doses of infliximab, the skin lesions and joint pain exacerbated and became intractable. Ten days after the dosage of infliximab was increased, the patient experienced headache and nausea with high fever. He had scaly, well-circumscribed erythemas on his trunk, extremities, and deformed nails. He also had swelling and pain in multiple joints. His complete blood and differential leukocyte counts were normal. The level of C-reactive protein was 16.66 mg/dL, whereas anti-infliximab antibodies were absent. Nuchal rigidity was absent and there were no abnormal neurological findings; however, jolt test results were positive. Results from magnetic resonance imaging were normal, whereas those from cerebrospinal fluid (CSF) examination were almost normal. The CSF contained mononuclear cells and was negative for bacteriological cultures, India ink staining, and polymerase chain reaction amplification of herpesvirus group DNA. Headache and nausea improved 2 months after infliximab was discontinued. The patient failed to respond to infliximab treatment for PsA, and we diagnosed infliximab-induced aseptic meningitis. Infliximab was discontinued and treatment with ustekinumab and methotrexate was initiated. Thereafter, the psoriatic skin lesion and joint pain gradually improved. Infliximab-induced aseptic meningitis may be a differential diagnosis when symptoms of meningitis develop during infliximab administration.


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