We aimed to determine the diagnostic performance of anti-BP180 IgG and anti-BP230 IgG in BP, to correlate disease activity with autoantibody levels through follow-ups, and to relate BP comorbidities with disease activity and autoantibody levels.
It is due to the formation of autoantibodies directed against different epitopes of bullous pemphigoid (BP) 180 as a consequence of the aberrant expression of BP180 in the placental tissue of genetically predisposed women.
Our aims were two-fold: 1) To establish the clinical relationships between total and BP180-specific IgE, eosinophilia and other markers of disease activity; and 2) To determine if eosinophils from BP patients express the high affinity IgE receptor, FcεRI, as a potential mechanism of action for IgE in BP.
We aimed to determine the diagnostic performance of anti-BP180 IgG and anti-BP230 IgG in BP, to correlate disease activity with autoantibody levels through follow-ups, and to relate BP comorbidities with disease activity and autoantibody levels.
We have subsequently found several lines of evidence suggesting a significant role of IL-17A in the BP pathogenesis: (i) IL-17A activated human neutrophils in vitro, (ii) inhibition of dermal-epidermal separation in cryosections of human skin incubated with anti-BP180 IgG and subsequently with anti-IL-17A IgG-treated leukocytes, (iii) close correlation of serum IL-17A levels and diseases activity in a mouse model of BP, (iv) IL17A-deficient mice were protected against autoantibody-induced BP, and (v) pharmacological inhibition of lL-17A reduced the induction of BP in mice.
Routine serological testing and follow-up of BP relies on indirect immunofluorescence (IIF) of serum Abs, commonly performed on monkey oesophagus (ME), and/or enzyme-linked immunosorbent assay (ELISA) testing on recombinantly produced fragments of BP180 and BP230 (BP180-NC16A, BP230-C/N).
These patients' demographic characteristics and BP180 and BP230 levels were compared with those of a BP control group who were positive for BP180 or BP230 autoantibodies and had positive DIF study findings.
These patients' demographic characteristics and BP180 and BP230 levels were compared with those of a BP control group who were positive for BP180 or BP230 autoantibodies and had positive DIF study findings.
To determine the effect of gliptins on the expression of the DPP-4/CD-26 protein we performed immunohistochemistry, which showed that the skin expression of DPP-4/CD-26 was increased in BP patients, but not affected by prior gliptin treatment.
Immunohistochemistry showed strong TWEAK and Fn14 expression and implied an opposite relationship between the TWEAK and BP180 expression in skin samples from BP patients.
We have found an association between BP, ND and specific serologic profile characterized by higher levels of anti-BP180 and anti-BP230 (t(45)=2.319, p=0.025 and t(45)= 2.486, p=0.017, respectively), as compared to BP patients without ND.
BPAG2 is physiologically and aberrantly expressed in neuronal tissue and internal malignancies, and the associations of BP with Parkinson's disease, stroke and internal malignancies invites new investigations into the immunological dysregulation behind the comorbidity.
We here addressed the influence of serum and blister fluid (BF) from patients with BP on the polarization status of macrophages with regards to the metalloproteinase-9 (MMP-9) expression.
In the present study we evaluated the expression of mRNA for IL-4, IL-5, TGF-beta1, IFN-gamma in CP in comparison to bullous pemphigoid (BP) patients, investigating the role of cytokine profile as possible cause of the different disease evolution.
CCL18 expression is up-regulated in lesional skin of atopic dermatitis and bullous pemphigoid, suggesting its important roles in the development of these skin diseases.