Search PubMed⌕ Search

Biomedical subjects

W R Gammon

Publications and source records attributed to W R Gammon.

85 records · Page 5Linked to original sources
PubMed1982

Double immunofluorescence microscopy: a method for localizing immune deposits in skin diseases associated with linear basement membrane zone immunofluorescence.

Direct immunofluorescence microscopy has shown that a linear pattern of immunoglobulin and/or complement deposition at the cutaneous basement membrane zone is a characteristic feature in a number of acquired bullous diseases and is occasionally observed in systemic lupus erythematosus. Immunoelectron microscopy has shown the linear pattern of immunofluorescence may be produced by immune deposits located either above the basal lamina (in the lamina lucida) or below the basal lamina (in the upper dermis). Distinguishing between these sites of immune reactant deposition may be of value in differential diagnosis. In this study we report a double immunofluorescent method by which skin biopsies with linear IgG immunofluorescence due to deposits above the basal lamina (bullous pemphigoid) could be distinguished from biopsies with deposits beneath the basal lamina (bullous systemic lupus erythematosus and epidermolysis bullosa acquisita). When skin sections were treated sequentially with rhodamine-labeled anti-human IgG followed by fluorescein-labeled antilamina lucida (pemphigoid) antibody and examined by fluorescence microscopy, the following results were obtained. In biopsies with IgG deposits in the lamina lucida, a single green fluorescent band was observed. In tissues with subbasal lamina deposits, either parallel and contiguous bands of green and yellow-orange fluorescence or a single band of yellow-orange fluorescence was observed. The method is simpler, quicker, and less expensive than immunoelectron microscopy and should be a useful technique for evaluating skin diseases with linear immunofluorescence at the basement membrane zone.

Basement Membrane↗
PubMed1982

An in vitro model of immune complex-mediated basement membrane zone separation caused by pemphigoid antibodies, leukocytes, and complement.

In this study, an in vitro model of immune complex-mediated basement membrane zone separation caused by periphigoid antibodies, serum complement, and peripheral blood leukocytes is described. When cryostat sections of fresh-frozen normal human skin were treated with either of 4 bullous pemiphigoid sera containing complement-activating anti-basement membrane zone antibodies and subsequently incubated at 37 degrees C with normal human peripheral blood leukocytes and fresh human serum, leukocytes attached to 96% of the basement membrane zone in 100% of sections. Sixty-seven percent of the sections developed focal areas of basement membrane zone separation resembling dermal-epidermal separation described in early pemphigoid lesions. In control sections in which either leukocytes, pemphigoid antibody or fresh human serum were omitted, significantly less leukocyte attachment and basement membrane zone separation occurred. Evidence that leukocytes caused separation was supported by an absolute requirement for viable leukocytes during incubation, a high correlation between leukocyte attachment and separation and experiments showing that leukocytes attached to the basement membrane zone were activated. This study provides the first in vitro evidence directly supporting a functional role for immune-complex mediated inflammation in the pathogenesis of basement membrane zone separation and blisters in bullous pemphigoid.

Antibodies↗
PubMed1980

Pemphigoid antibody mediated attachment of peripheral blood leukocytes at the dermal-epidermal junction of human skin.

It has been proposed that cutaneous inflammation and blister formation in bullous pemphigoid is caused by antibodies to the cutaneous basement membrane zone which active complement, thereby, attracting leukocytes to the dermal-epidermal junction. There is, however, no functional evidence which supports a role for pemphigoid antibodies in complement activation or leukocyte activity in skin. This study describes the in vitro attachment of human peripheral blood leukocytes to the dermal-epidermal junction of cryostat skin sections treated with 9/13 pemphigoid sera containing antibodies to the cutaneous basement membrane zone. A requirement for complement in the reaction was supported by the findings that only complement-fixing pemphigoid sera mediated the leukocyte response, a strong correlation existed between complement-fixation titers and leukocyte attachment titers and only leukocytes suspended in fresh serum but not buffer or heat inactivated serum attached at the junction. A requirement for antibody was supported by the observation that IgG fractions of 4 pemphigoid sera were as effective as whole sera in mediating leukocyte attachment. The leukocyte response was shown to be specific for complement-fixing pemphigoid sera since it was not observed with noncomplement-fixing sera or sera from 15 normal human and 22 nonpemphigoid disease controls. This study offers functional evidence for an interaction between pemphigoid antibody, complement and leukocytes in the immunopathogenesis of bullous pemphigoid and demonstrates that complement-fixing antibasement membrane zone antibodies may be important in initiating the cellular inflammatory events observed near the dermal-epidermal junction in vivo.

Adult↗
PubMed1979

Urticarial vasculitis: report of a case and review of the literature.

A woman with cutaneous vasculitis had a severe bullous eruption that was suggestive of erythema multiforme. The patient also had a history of recurrent urticaria that continued intermittently for over a year of follow-up examination. Skin biopsy specimens of both urticarial and erythema and multiforme lesions showed leukocytoclastic vasculitis. An illness resembling systemic lupus erythematosus (SLE) is suggested by transient, low-titer, positive antinuclear antibody tests, persistent deposits of immunoglobulin and complement in normal skin, arthralgias, circulating immune complexes, and chronic hypocomplementemia. This case is similar to cases previously reported as "hypocomplementemic vasculitis," an "unusual SLE-related syndrome," and "urticaria with vasculitis."

Adult↗
PubMed1979

Cutaneous plasmacytomas. A review and presentation of an unusual case.

Recent reviews separate four types of plasma cell tumor: multiple myeloma, extramedullary plasmacytoma (without multiple myeloma), solitary myeloma of bone, and plasma cell leukemia. Cutaneous plasma cell tumors may arise from lymphatic or vascular spread of tumor (metastatic cutaneous plasmacytoma) or by direct extension from bone lesions. The former, metastatic cutaneous plasmacytomas, are quite rare. Specific malignant plasmacyte cutaneous tumors can also be seen in extramedullary plasmacytoma, solitary myeloma of bone, and plasma cell leukemia. We present a patient with multiple myeloma and lymphedema of the right arm, who developed a pathologic fracture of the right humerus and subsequently developed numerous metastatic cutaneous plasmacytomas localized to the lymphedematous arm. Direct immunofluorescence of frozen sections and enzymatically released cells from tumor nodule failed to reveal cell-associated immunoglobulins.

Female↗
PubMed1979

Demonstration of the complement regulating protein, beta 1H, in skin biopsies from patients with bullous pemphigoid.

beta 1H-globulin is a recently characterized plasma protein which regulates the biologic activities of the major fragment of the third complement component, C3b. The major function of this protein is to act as a co-factor for C3b Inactivator (C3bINA) in the cleavage of C3b to an intermediate molecule, C3b', consisting of an intact beta-chain covalently bound by disulfide bridges to 2 alpha-chain fragments of 40,000 and 67,000 daltons. Final cleavage of C3b' to the C3c and C3d fragments requires an additional protease such as plasmin or elastase. Additionally, beta 1H interferes with the activity of the alternative pathway convertases, C3bBb and C3bBbP, by displacing or competing with the binding of factor B. In this study, perilesional skin biopsies from 10 patients with active bullous pemphigoid were examined for the presence of beta 1H at the dermal-epidermal junction by immunofluorescent methods. The protein was found in 8 of 9 biopsies in which C3 also was deposited. In a single case where C3 was not found, beta 1H was not seen. These findings suggest that beta 1H plays a role in the in vivo control of C3b and provides additional evidence for the participation of the complement system in the pathogenesis of bullous pemphigoid.

Aged↗
PubMed1978

Secondary cutaneous mucinosis with systemic lupus erythematosus. A case presentation and review of the literature.

A patient had papular and nodular cutaneous deposits of mucin and cutaneous and systemic manifestations of lupus erythematosus (LE). Since many of the mucinous deposits occurred at sites that were clinically free of skin lesions of LE, we considered initially that the patient had both LE and papular mucinosis. However, after a review of the English literature and further study of the patient, it seemed more likely that the papular and nodular deposits of mucin were secondary to LE and not a previously unreported simultaneous occurrence of the two diseases in the same patient. To our knowledge, this is the third case report of a patient with papular and nodular cutaneous mucinosis secondary to LE. In addition to the case report, this article is concerned with a discussion of cutaneous mucinosis in LE and other "collagen vascular" diseases.

Adult↗