Cytotoxic T lymphocytes and phenotypically abnormal epidermal dendritic cells in fixed cutaneous eruptions

Murphy, Gëorge F.; Guillén, Francisco J.; Flynn, Timothy C.

doi:10.1016/s0046-8177(85)80040-x

Cited by 12 publications

(9 citation statements)

References 18 publications

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“…Previous studies have led to the conclusions that FDE represent a type of cellmediated hypersensitivity reaction, mediated by T lymphocytes (11). Murphy et al speculated that the HLA-DR positivity of keratinocytes in FDE is due to the release of gamma-interferon (11). We have investigated whether cell-mediated immunity is involved in the pathogenesis of FDE by examining whether or not there is an increase in the cytokineinducible protein, IP-10 in these lesions.…”

Section: Discussionmentioning

confidence: 96%

“…Subsequent exposures to the antigen may elicit more widespread, though still locaHzed cutaneous disease, since internal involvement has not been described in FDE (24). Previous studies have led to the conclusions that FDE represent a type of cellmediated hypersensitivity reaction, mediated by T lymphocytes (11). Murphy et al speculated that the HLA-DR positivity of keratinocytes in FDE is due to the release of gamma-interferon (11).…”

Section: Discussionmentioning

confidence: 99%

“…In addition. Murphy et al (11) found increased HLA-DR expression on keratinocytes and suggested that this represented evidence for local gamma interferon production by activated lymphocytes. IP-10 is a cytokine expressed by keratinocytes, as well as endothelial cells and mononuclear cells following exposure to gamma interferon (14).…”

mentioning

confidence: 99%

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Fixed drug eruptions: evidence for a cytokine‐mediated process

Smoller¹,

Luster

Krane

et al. 1991

J Cutan Pathol

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Fixed drug eruptions (FDE) are immunologic reactions to drugs which produce erythematous plaques or blisters that characteristically recur at the same cutaneous sites with repeated antigenic challenges. While a detailed pathogenesis of these lesions remains obscure, T-lymphocyte infiltration has been documented repeatedly. In this study, we tried to determine if FDE were mediated, at least in part, by cytokines, such as gamma-interferon. We examined biopsies from 6 cases of clinically well-documented FDE with an HLA-DR antibody, LN3, and an antibody to gamma IP-10 (IP-10), a protein expressed by keratinocytes, monocytes, lymphocytes and endothelial cells following exposure to gamma-interferon. We found staining of the dermal lymphocytes with anti-HLA-DR antibody in all 6 cases examined. Keratinocytes and endothelial cells showed only focal staining at the antibody concentrations used. In addition, there was keratinocyte staining with the IP-10 antibody at all levels of the epidermis, with accentuation in areas of blister formation. There was more intense staining of keratinocytes with the IP-10 antibody in cases with accumulations of HLA-DR positive lymphocytes in the dermis. We believe that these findings are consistent with the hypothesis that FDE represent cell-mediated immunologic responses to a variety of antigens, and further, that the histologic alterations can be explained, at least in part, by a cytokine-mediated process.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

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Fixed drug eruptions: evidence for a cytokine‐mediated process

Smoller¹,

Luster

Krane

et al. 1991

J Cutan Pathol

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“…4. In bronchial provocation tests, unspecific stimuli like acetyl (or methyl) choline, histamine, dust, cold air, exercise or hyperventilation are used [1,2,13,18,34,37,41]. The following test concentrations are used: acetylcholine (1.0 -100 mg/ml); methylcholine (0.05 -50 mg/ml); carbamylcholine (0.05 -50 mg/ml); histamine (0.05 -50 mg/ml) [17].…”

Section: Diagnosismentioning

confidence: 99%

“…General rule: The more severe the anaphylactic symptoms to be expected, the sooner they will become manifest! Of course, there are exceptions from the rule in the form of "tricky" late anaphylactic reactions after several hours [31,41]; often, however, mild symptoms occur within the first 20 min which tend to be overlooked.…”

Section: Prophylaxis and Therapymentioning

confidence: 99%

Allergic Diseases (and Differential Diagnoses)

2005

Allergy in Practice

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There are many allergic diseases manifesting in different organs and on the basis of different pathomechanisms (see Sect. 1.3). The most common allergies develop via IgE antibodies and manifest within minutes to hours after allergen contact ("immediate-type reactions"). Not infrequently, there are biphasic (dual) reaction patterns when after a strong immediate reaction in the course of 6-12 h a renewed hypersensitivity reaction (late-phase reaction, LPR) occurs which is triggered by IgE, but amplified by recruitment of additional cells and mediators. These LPRs have to be distinguished from classic delayed-type hypersensitivity (DTH) reactions (type IV reactions) (see Sect. 5.5).What may be confusing for the inexperienced physician is familiar to the allergist: The same symptoms of immediate-type reactions are observed without immune phenomena (skin tests or IgE antibodies) being detectable. These reactions are called "pseudo-allergic reactions" (PARs), the term "pseudo" only reflecting the not detectable participation of the immune system and not implying "psychological" phenomena. People can die from pseudoallergic reactions! The term is negatively defined; with better techniques allowing the detection of antibodies or sensitized cells, PAR may turn into true allergy. IgE-mediated drug allergies will be covered together with other adverse drug reactions (see Sect. 5.7).In atopic eczema, IgE antibodies play a role in many patients in the eliciting phase, albeit in close connection with T-cell-mediated reac-tions (combination of type I and type IV b reactions). Atopic eczema will be discussed in a separate section (see Sect. 5.5.3).The maximal manifestation of IgE-mediated immediate-type allergic reaction is anaphylaxis. In the development of clinical symptoms, different organs may be involved and symptoms of well-known allergic diseases of skin and mucous membranes [also called "shock fragments" (Karl Hansen)] may occur according to the severity (see Sect. 5.1.4).

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T-Cell Subsets in Drug-Induced Toxic Epidermal Necrolysis

Miyauchi¹

1991

Arch Dermatol

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A patient with bromisovalum-induced toxic epidermal necrolysis showed pronounced delayed hypersensitivity to bromisovalum by patch testing. Biopsy specimens from the cutaneous lesion and the site of the positive patch test reaction were analyzed and compared immunohistologically. The findings were similar: most of the mononuclear cells disposed along the dermoepidermal junction and migrating into the epidermis were CD8-positive lymphocytes, whereas the dermal inflammatory infiltrates were composed predominantly of CD4-positive lymphocytes. This case showed the potential usefulness of patch testing in evaluating cases of toxic epidermal necrolysis. We believe that delayed hypersensitivity plays a crucial role in the development of drug-induced toxic epidermal necrolysis. Furthermore, potential effector cells with phenotypic characteristics of CD8-positive lymphocytes (suppressor/cytotoxic T cells) seem to represent important mediators of the epidermal damage of the cutaneous lesion in our case.

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Cytotoxic T lymphocytes and phenotypically abnormal epidermal dendritic cells in fixed cutaneous eruptions

Cited by 12 publications

References 18 publications

Fixed drug eruptions: evidence for a cytokine‐mediated process

Fixed drug eruptions: evidence for a cytokine‐mediated process

Allergic Diseases (and Differential Diagnoses)

T-Cell Subsets in Drug-Induced Toxic Epidermal Necrolysis

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