scholarly journals comment:Cytotoxic and antigen presenting cells, and non-basement membrane zone pathology in a case of bullous pemphigoid

2012 ◽  
Vol 3 (2) ◽  
pp. 100-101
Author(s):  
Sho Hiroyasu ◽  
Daisuke Tsuruta
Keyword(s):  
Basement Membrane ◽  
Bullous Pemphigoid ◽  
Antigen Presenting Cells ◽  
Basement Membrane Zone ◽  
Antigen Presenting

scholarly journals Stratification of Antigen-presenting Cells within the Normal Cornea

2009 ◽  
Vol 1 ◽  
pp. OED.S2813 ◽  
Author(s):  
Jared E. Knickelbein ◽  
Simon C. Watkins ◽  
Paul G. Mcmenamin ◽  
Robert L. Hendricks
Keyword(s):  
Bone Marrow ◽  
Basement Membrane ◽  
Mhc Class Ii ◽  
Fluorescent Protein ◽  
Antigen Presenting Cells ◽  
Class Ii ◽  
Apical Surface ◽  
Bone Marrow Derived Cells ◽  
Green Fluorescent ◽  
Antigen Presenting

The composition and location of professional antigen presenting cells (APC) varies in different mucosal surfaces. The cornea, long considered an immune-privileged tissue devoid of APCs, is now known to host a heterogeneous network of bone marrow-derived cells. Here, we utilized transgenic mice that express enhanced green fluorescent protein (EGFP) from the CD 11c promoter (pCD11c) in conjunction with immunohistochemical staining to demonstrate an interesting stratification of APCs within non-inflamed murine corneas. pCD11c+ dendritic cells (DCs) reside in the basal epithelium, seemingly embedded in the basement membrane. Most DCs express MHC class II on at least some dendrites, which extend up to 50 μm in length and traverse up 20 μm tangentially towards the apical surface of the epithelium. The DC density diminishes from peripheral to central cornea. Beneath the DCs and adjacent to the stromal side of the basement membrane reside pCD11c–CD11b+ putative macrophages that express low levels of MHC class II. Finally, MHC class II–pCD11c–CD11b+ cells form a network throughout the remainder of the stroma. This highly reproducible stratification of bone marrow-derived cells is suggestive of a progression from an APC function at the exposed corneal surface to an innate immune barrier function deeper in the stroma.

scholarly journals Gelatinase B–deficient Mice Are Resistant to Experimental Bullous Pemphigoid

1998 ◽  
Vol 188 (3) ◽  
pp. 475-482 ◽  
Author(s):  
Zhi Liu ◽  
J. Michael Shipley ◽  
Thiennu H. Vu ◽  
Xiaoye Zhou ◽  
Luis A. Diaz ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Bullous Pemphigoid ◽  
Neutrophil Infiltration ◽  
Basement Membrane Zone ◽  
Neutrophil Recruitment ◽  
Gelatinase B ◽  
Collagen Xvii ◽  
Blistering Disease ◽  
Novel Therapeutic Strategies ◽  
Deficient Mice

Bullous pemphigoid (BP) is an autoimmune subepidermal blistering disease characterized by deposition of autoantibodies at the basement membrane zone. In an experimental BP model in mice, the subepidermal blistering is mediated by antibodies directed against the hemidesmosomal protein BP180 (collagen XVII, BPAG2), and depends on complement activation and neutrophil infiltration. Gelatinase B is present in BP blister fluid and can cleave BP180. In this study we investigated the role of gelatinase B in the immunopathogenesis of experimental BP using mice containing targeted disruption of the gelatinase B (MMP-9, 92 kD gelatinase) gene. Gelatinase B–deficient mice were resistant to the blistering effect of intracutaneous anti-mBP180 antibodies, although these mice showed deposition of autoantibodies at the basement membrane zone and neutrophil recruitment to the skin comparable to that observed in the control mice. Interleukin 8 given intradermally concomitantly with pathogenic anti-mBP180 elicited a significant neutrophil recruitment into the skin in gelatinase B–deficient mice, but blistering did not occur. However, gelatinase B–deficient mice reconstituted with neutrophils from normal mice developed blistering in response to anti-mBP180 antibodies. These results implicate neutrophil-derived gelatinase B in the pathogenesis of experimental BP and might lead to novel therapeutic strategies for BP.

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