Serum Soluble CD200 Level was Higher in Patients with Bullous Pemphigoid During the Active Phase of the Disease than for Healthy Individuals

Akman-Karakaş, Ayşe; Yalçın, Arzu Didem; Koç, Saliha; Gümüşlü, Saadet; Ergun, Erkan; Genc, Gizem Esra; Öngüt, Gözde; Uzun, Soner; Alpsoy, Erkan

doi:10.7754/clin.lab.2013.130744

Cited by 6 publications

(3 citation statements)

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“…The extracellular portion of CD200 once cleaved is released into the extracellular matrix as bio-actively soluble CD200 (sCD200) (78). Circulating levels of sCD200 have also been found to correlate with disease severity in a number of inflammatory diseases, such as systemic lupus erythematosus, endometriosis and bullous pemphigoid (79)(80)(81). ADAM 28 has previously been shown to be responsible for sCD200 release in chronic lymphocytic leukaemia (78).…”

Section: Discussionmentioning

confidence: 99%

CD200 ectodomain shedding into the tumor microenvironment leads to NK cell dysfunction and apoptosis

Morgan¹,

Rees²,

Lanfredini³

et al. 2022

Journal of Clinical Investigation

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The basis of immune evasion, a hallmark of cancer, can differ even when cancers arise from one cell type such as in the human skin keratinocyte carcinomas: basal and squamous cell carcinoma. Here we showed that the basal cell carcinoma tumor initiating cell surface protein CD200, through ectodomain shedding, was responsible for the near absence of NK cells within the basal cell carcinoma tumor microenvironment. In situ, CD200 underwent ectodomain shedding by metalloproteinases MMP3 and MMP11, which released biologically active soluble CD200 into the basal cell carcinoma microenvironment. CD200 bound its cognate receptor on NK cells, to suppress MAPK pathway signaling that in turn blocked indirect (gamma interferon release) and direct cell killing. In addition, reduced ERK phosphorylation relinquished negative regulation of PPARγ regulated gene transcription and lead to membrane accumulation of the Fas/FADD death receptor and its ligand, FasL that resulted in activation-induced apoptosis. Blocking CD200 inhibition of MAPK or PPARγ signaling restored NK cell survival and tumor cell killing, with relevance to many cancer types. Our results thus uncover a paradigm for CD200 as a potentially novel and targetable NK cell specific immune checkpoint, which is responsible for NK cell associated poor outcomes in many cancers.

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Section: Discussionmentioning

confidence: 99%

CD200 ectodomain shedding into the tumor microenvironment leads to NK cell dysfunction and apoptosis

Morgan¹,

Rees²,

Lanfredini³

et al. 2022

Journal of Clinical Investigation

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“…Recent reports revealed that patients with CU also show signs of thrombin generation and activation of the TF pathway of the coagulation system. DD, a fibrin degradation product formed during the lysis of a thrombus is also detected in high levels in patients with active CU [62][63][64][65][66]. After Omalizumab therapy, significant decrease of the levels of DD shows the importance of procoagulant state in allergic patients.…”

Section: Omalizumab Effects On Coagulation Pathwaymentioning

confidence: 96%

ANTI-Ige: An Overview

Yalçın¹

2014

Glob J Allergy

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Asthma is common chronic inflammatory disease of the airways characterised by variable and attacks of cough and breathlesness, usually precipitated by an enviromental trigger (air pollution, smoke, etc). The prevalence and severity for allergic asthma have increased markedly in the last several decades. Dysregulated expression patterns of pro-and anti inflammatory mechanisms are thought to be responsible for the development of chronic inflammation. The risk of developing asthma has a strong genetic component, with estimated heritability ranging from 35 to 85%. The mechanism of action of Omalizumab in the treatment of asthma is believed to be multifactorial.

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“…Reduction in serum levels sOX-2 with anti-IgE treatment suggests that sOX-2 could be pro-inflammatory [ 11 , 14 , 37 , 47 , 48 ]. Soluble OX-2 might also play a role in immune response in the pathogenesis of autoimmune and inflammatory skin disorders [ 50 , 51 ].…”

Section: Omalizumab Effects On Scd200 (Ox-2)mentioning

confidence: 99%

An Overview of the Effects of anti-IgE Therapies

Yalçın

2014

Med Sci Monit

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Source of support:Self financing Omalizumab, a humanized mAb that binds to the CH3 domain near the binding site for the high-affinity type-I IgE Fc receptors of human IgE, can neutralize free IgE and inhibit the IgE allergic pathway without sensitizing mast cells and basophils. We found that omalizumab in patients with severe persistent asthma (SPA) was an effective therapy for asthma and the following co-morbid conditions: chronic urticaria (CU), bee venom allergy, latex allergy, atopic dermatitis, food allergy and Samter's syndrome. Information on the use of omalizumab in treatment of asthma and other allergic diseases has improved our understanding that treatment acts on many levels, including regulating levels of inflammatory proteins, including cytokines (copper-containing alpha-2-glycoprotein, total antioxidant capacity, MDA, NO, H 2 O 2 , CXCL8, IL-10, TGF-b, GMCSF, IL-17, IL-1b), MPV, Hs-CRP, eosinophil cationic peptide, vitamin-D (25(OH)D), homocysteine (Hcy), OX-2, d-dimer, albumin, and sApo-2L. The decrease in Hcy concentrations and increase in 25(OH)D also support the existence of a vascular endothelial protection mechanism. Mediators and cells classically involved in pro-coagulant and anticoagulant pathways together play a role in SPA and CU pathophysiology and omalizumab effect. The mechanism of action of omalizumab in the treatment of asthma is believed to be multifactorial, and includes effects mediated through altered production of redox metabolites, extrinsic coagulation pathway, oxidative markers-related mi RNA, TRAIL-related mi RNA, and regulation of production of known inflammatory proteins BackgroundOmalizumab -anti-immunoglobulin E (IgE) -is approved for the treatment of severe allergic asthma. In addition to asthma, Omalizumab has been investigated in various other conditions, including chronic urticaria (CU), perennial and seasonal allergic rhinitis (AR), latex allergy, peanut allergy, idiopathic anaphylaxis, hyper-IgE syndrome, chronic rhinosinusitis, interstitial cystitis, aspirin sensitivity, mastocytosis, eosinophilic gastroenteritis, and atopic dermatitis [1,2]. Omalizumab -a humanized mAb that binds to the CH3 domain near the binding site for the high-affinity type-I IgE Fc receptors of human IgE -can neutralize free IgE and inhibit the IgE allergic pathway without sensitizing mast cells and basophils. It is conceivable that mast cells residing in the nasal lining, lower airway, other areas of the mucosal tracts, and in the skin, differ in tryptase and chymase content, sensitivity, receptor regulation, and life span [3][4][5][6][7][8]. The development of Omalizumab therapy over the past 20 years provides an interesting example of the emergence of a conceptually new, biotechnologyproduced pharmaceutical [8]. Omalizumab and IgE ReceptorsThe potential for Omalizumab to exert anti-inflammatory effects in patients with asthma arises from its ability to target the interaction between IgE and IgE receptors (FceRI and FceRII), thereby preventing inflammatory cell activation and interrupti...

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Serum Soluble CD200 Level was Higher in Patients with Bullous Pemphigoid During the Active Phase of the Disease than for Healthy Individuals

Cited by 6 publications

References 0 publications

CD200 ectodomain shedding into the tumor microenvironment leads to NK cell dysfunction and apoptosis

CD200 ectodomain shedding into the tumor microenvironment leads to NK cell dysfunction and apoptosis

ANTI-Ige: An Overview

An Overview of the Effects of anti-IgE Therapies

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