Type XVII collagen (BP180) can function as a cell−matrix adhesion molecule via binding to laminin 332

Bergh, Françoise Van den; Eliason, Steven; Giudice, George J.

doi:10.1016/j.matbio.2010.10.005

Cited by 46 publications

(32 citation statements)

References 34 publications

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“…In vivo subepidermal blistering is observed when expression of BP180 is reduced or absent because of gene knockout in mice or mutation in humans with generalized atrophic benign epidermolysis bullosa (6,49). Van den Bergh and colleagues (50) demonstrated that in cells that lack other hemidesmosomal components, cell matrix attachment is directly related to the amount of BP180 expression. In this study, we demonstrate that BP autoantibodies decrease confluence of cultured keratinocytes and the number of hemidesmosomes localized at the BMZ of organ cultured skin.…”

Section: Discussionmentioning

confidence: 99%

FcR-Independent Effects of IgE and IgG Autoantibodies in Bullous Pemphigoid

Messingham

Srikantha

DeGueme

et al. 2011

The Journal of Immunology

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Bullous pemphigoid (BP) is a subepidermal blistering disease characterized by IgE and IgG class autoantibodies specific for 180-kDa BP Ag 2 (BP180), a protein involved in cell-substrate attachment. Although some direct effects of BP IgG have been observed on keratinocytes, no study to date has examined direct effects of BP IgE. In this study, we use primary cultures of human keratinocytes to demonstrate Ag-specific binding and internalization of BP IgE. Moreover, when BP IgE and BP IgG were compared, both isotypes stimulated FcR- independent production of IL-6 and IL-8, cytokines critical for BP pathology, and elicited changes in culture confluence and viability. We then used a human skin organ culture model to test the direct effects of these Abs on the skin, whereas excluding the immune inflammatory processes that are triggered by these Abs. In these experiments, physiologic concentrations of BP IgE and BP IgG exerted similar effects on human skin by stimulating IL-6 and IL-8 production and decreasing the number of hemidesmosomes localized at the basement membrane zone. We propose that the Ab-mediated loss of hemidesmosomes could weaken attachment of basal keratinocytes to the basement membrane zone of affected skin, thereby contributing to blister formation. In this article, we identify a novel role for IgE class autoantibodies in BP mediated through an interaction with BP180 on the keratinocyte surface. In addition, we provide evidence for an FcR-independent mechanism for both IgE and IgG class autoantibodies that could contribute to BP pathogenesis.

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Section: Discussionmentioning

confidence: 99%

FcR-Independent Effects of IgE and IgG Autoantibodies in Bullous Pemphigoid

Messingham

Srikantha

DeGueme

et al. 2011

The Journal of Immunology

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“…The protein contributes to keratinocyte adhesion by interacting with extracellular matrix proteins such as laminin 332 (Fig. 3b) (105,106).…”

Section: Bullous Pemphigoid and Its Target Autoantigensmentioning

confidence: 99%

One gene but different proteins and diseases: the complexity of dystonin and bullous pemphigoid antigen 1

Künzli

Favre

Chofflon³

et al. 2015

Experimental Dermatology

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Since the immunochemical identification of the bullous pemphigoid antigen 230 (BP230) as one of the major target autoantigens of bullous pemphigoid (BP) in 1981, our understanding of this protein has significantly increased. Cloning of its gene, development and characterization of animal models with engineered gene mutations or spontaneous mouse mutations have revealed an unexpected complexity of the gene encoding BP230. The latter, now called dystonin (DST), is composed of at least 100 exons and gives rise to three major isoforms, an epithelial, a neuronal and a muscular isoform, named BPAG1e (corresponding to the original BP230), BPAG1a and BPAG1b, respectively. The various BPAG1 isoforms play a key role in fundamental processes, such as cell adhesion, cytoskeleton organization, and cell migration. Genetic defects of BPAG1 isoforms are the culprits of epidermolysis bullosa and complex, devastating neurological diseases. In this review, we summarize recent advances of our knowledge about several BPAG1 isoforms, their role in various biological processes and in human diseases.

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“…It is notable that some interactions between cell-associated receptors and collagens occur indirectly as, for instance, in the case of the platelet receptor GP I that interacts with collagens by the intermediate of von Willebrand Factor (vWF) (Leitinger & Hohenester, 2007). Finally, it is important to mention that some collagens (XIII, XVII, XXIII and XXV) act themselves as membrane receptors to components of the BM like Ln or collagen IV (Qiao et al, 2009;Van den Bergh et al, 2011).…”

Section: Functions and Distributionmentioning

confidence: 99%

Human pathogens utilize host extracellular matrix proteins laminin and collagen for adhesion and invasion of the host

et al. 2012

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Laminin (Ln) and collagen are multifunctional glycoproteins that play an important role in cellular morphogenesis, cell signalling, tissue repair and cell migration. These proteins are ubiquitously present in tissues as a part of the basement membrane (BM), constitute a protective layer around blood capillaries and are included in the extracellular matrix (ECM). As a component of BMs, both Lns and collagen(s), thus function as major mechanical containment molecules that protect tissues from pathogens. Invasive pathogens breach the basal lamina and degrade ECM proteins of interstitial spaces and connective tissues using various ECM-degrading proteases or surface-bound plasminogen and matrix metalloproteinases recruited from the host. Most pathogens associated with the respiratory, gastrointestinal, or urogenital tracts, as well as with the central nervous system or the skin, have the capacity to bind and degrade Lns and collagen(s) in order to adhere to and invade host tissues. In this review, we focus on the adaptability of various pathogens to utilize these ECM proteins as enhancers for adhesion to host tissues or as a targets for degradation in order to breach the cellular barriers. The major pathogens discussed are Streptococcus, Staphylococcus, Pseudomonas, Salmonella, Yersinia, Treponema, Mycobacterium, Clostridium, Listeria, Porphyromonas and Haemophilus; Candida, Aspergillus, Pneumocystis, Cryptococcus and Coccidioides; Acanthamoeba, Trypanosoma and Trichomonas; retrovirus and papilloma virus.

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Type XVII collagen (BP180) can function as a cell−matrix adhesion molecule via binding to laminin 332

Cited by 46 publications

References 34 publications

FcR-Independent Effects of IgE and IgG Autoantibodies in Bullous Pemphigoid

FcR-Independent Effects of IgE and IgG Autoantibodies in Bullous Pemphigoid

One gene but different proteins and diseases: the complexity of dystonin and bullous pemphigoid antigen 1

Human pathogens utilize host extracellular matrix proteins laminin and collagen for adhesion and invasion of the host

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