Diagnostic utility of plasmacytoid dendritic cells in dermatopathology

Bardawil, Tara; Khalil, Samar; Kurban, Mazen; Abbas, Ossama

doi:10.25259/ijdvl_638_19

Cited by 7 publications

(13 citation statements)

References 44 publications

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“…Finally, we screened six differentially expressed genes from 139 immune-related genes with lower expression in the sensitive group. CD123 can function as a specific marker to identify plasmacytoid DCs in tissue which might produce type I IFNs and be a tool in distinguishing dermatosis with overlapping characteristics such as lupus and its mimics [30][31][32]. CD103 is an integrin on the cell membrane, and CD8+CD103+ T regulatory cells (iTregs) can ameliorate excessive autoimmune inflammation and display therapeutic functions in lupus nephritis and other autoimmune diseases [33][34][35].…”

Section: Discussionmentioning

confidence: 99%

Systemic lupus erythematosus patients contain B‐cell receptor repertoires sensitive to immunosuppressive drugs

Pan

Chen

et al. 2022

Eur J Immunol

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Immune repertoire (IR) during treatment may be a surrogate biomarker for disease response. Changes of the IR in systemic lupus erythematosus patients in response to immunosuppressive drugs were identified in ten SLE patients. Patients provided peripheral blood mononuclear cells at two time points for sequencing. They were divided into sensitive and nonsensitive groups by their clinical responses to immunosuppressive drugs. After treatment, the BCR expression significantly decreased in patients from the sensitive group while there was no change in patients from the nonsensitive group. IgM comprised a dominant portion of the BCR repertoire and increased slightly in all patients in the sensitive group but decreased in the nonsensitive group. IgA also exhibited opposing changes between the two groups. Shorter CDR3 of TRB and TRG chains occurred in the sensitive group. CDR3 length of IGK decreased significantly in the sensitive group. CDR3 of TCR δ/γ changed distinctly between time points in the sensitive group. Six immunerelated genes showed differential expression levels in sensitive and nonsensitive groups.Our study shows that it is BCR repertoire sensitivity to immunosuppressive drugs in SLE patients and sheds light on personalized therapy for SLE.

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Section: Discussionmentioning

confidence: 99%

Systemic lupus erythematosus patients contain B‐cell receptor repertoires sensitive to immunosuppressive drugs

Pan

Chen

et al. 2022

Eur J Immunol

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“…31,32 MxA is used as a surrogate marker for type 1 interferon exposure. 17 In InfAIGA, a small number of TCL+ pDCs were localized near CTLs (data not shown). Sweat ducts in epidermal and dermal regions of anhidrotic skin are significantly exposed to type 1 interferons.…”

Section: Type 1 Interferon Signaturementioning

confidence: 87%

“…CXCR3 is expressed on CTLs and specifically binds to CXC motif chemokine ligand 10 (IP10/CXCL10), which is upregulated by type 1 interferons in sweat ducts and endothelium 15,16 . Myxovirus resistance protein A (MxA) can be used as a surrogate marker for type 1 interferon activity 15,17 …”

Section: Introductionmentioning

confidence: 99%

“…15,16 Myxovirus resistance protein A (MxA) can be used as a surrogate marker for type 1 interferon activity. 15,17 To objectively evaluate sweat coil atrophy, morphometric analysis and clear cell-specific IHC analysis using CAII were performed since sweat coil atrophy is largely caused by clear cell injury. 10 Here, we report features of the most common type of AIGA, namely inflammatory AIGA (InfAIGA), including the anatomical location of the inflammation, events associated with AIGA inflammation, and cell types involved.…”

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confidence: 99%

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Type 1 interferon signature and cytotoxic T lymphocyte activation targeted against sweat ducts in inflammatory acquired idiopathic generalized anhidrosis

Sano¹,

Asahina

Araki

et al. 2023

Acad Dermatol Venereol

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BackgroundAcquired idiopathic generalized anhidrosis (AIGA) leads to heat intolerance due to the loss or reduction in thermoregulatory sweating over an extensive area of the body. The pathomechanism of AIGA is still unclear but is believed to be autoimmune.ObjectivesWe investigated the clinical and pathological features of inflammatory AIGA (InfAIGA) and noninflammatory AIGA (non‐InfAIGA) within the skin.MethodsWe compared anhidrotic and normohidrotic skin samples from 30 patients with InfAIGA and non‐InfAIGA, as well as skin samples of melanocytic nevus as a negative control. We conducted morphometric analysis and immunohistochemical analysis of cell types and expression of inflammatory molecules (TIA1, CXCR3 and MxA). MxA expression was used as a proxy for type 1 interferon activity.ResultsWe found that tissue samples from patients with InfAIGA exhibited inflammation within the sweat duct and atrophy of the sweat coil, whereas patients with non‐InfAIGA exhibited only atrophy of the sweat coil. Cytotoxic T lymphocyte infiltration and MxA expression were only observed in the sweat ducts of patients with InfAIGA.ConclusionsInfAIGA is associated with increased sweat duct inflammation and sweat coil atrophy, whereas non‐InfAIGA is only associated with sweat coil atrophy. These data suggest that inflammation leads to epithelial destruction of sweat ducts associated with the sweat coil atrophy and subsequent loss of function. Non‐InfAIGA may be regarded as a postinflammatory state of InfAIGA. These observations indicate the contribution of both type 1 and type 2 interferons to sweat gland injury. The mechanism involved is similar to the pathomechanism of alopecia areata (AA).

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“…PDCs produce type 1 interferons in response to endogenous immune complex and play a crucial role in initiating inflammation in systemic autoimmune disease [29,50]. Additionally, PDCs may infiltrate the skin in severe infections (especially viral) and neoplastic entities [51,52]. The distribution and pattern of CD123+ PDCs have been documented in a variety of inflammatory dermatoses and noted in many forms of cutaneous lupus erythematosus, but have never been studied in OLE [19][20][21][22][23][24][25][26][27][28][29].…”

Section: Discussionmentioning

confidence: 99%

Comparative Analyses of Clinical Features, Histopathology, and CD123 Immunohistochemistry of Oral Lupus Erythematosus, Lichen Planus, and Other Lichenoid Lesions

Chanprapaph¹,

Pomsoong²,

Tankunakorn³

et al. 2021

Dermatology

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Background: Oral lupus erythematosus (OLE) and oral lichen planus (OLP) are among the common causes of oral lichenoid lesions (OLLs). The differential diagnosis among causes of OLLs, particularly between OLE and OLP, is challenging as they have significant clinical and histopathological overlap. Objectives: To compare and summarize the clinical, histopathological, and direct immunofluorescence (DIF) findings between OLE, OLP, and other OLLs and to explore the diagnostic value of CD123 immunohistochemistry. Methods: A retrospective study on patients with OLE, OLP, and other OLLs was performed between January 2014 and December 2019. The baseline characteristics, the clinical, histopathological, and DIF features, as well as CD123 immunohistochemistry for plasmacytoid dendritic cells (PDCs) were statistically analyzed and compared between groups. Results: Of 70 patients, 12 had OLE, 39 had OLP, and 19 had other OLLs. Oral erosions/ulcers were the most common findings in all three groups. Red macules, telangiectases, and discoid plaques were more common in OLE patients, while OLP cases were typified by reticulated patches (p < 0.05). Additionally, white patches were found more often in other OLLs than in both OLE and OLP (p = 0.002). Histologically, mucosal atrophy, basal vacuolization, and perivascular infiltrate were observed in OLE, whereas OLP specimens possessed mucosal hyperplasia, hypergranulosis, and compact orthokeratosis (p < 0.05). Mucosal spongiosis was a histologic feature that favored other OLLs over OLE and OLP (p < 0.001). Data on DIF were nonspecific for all three conditions. For immunohistochemical staining, the median number of total CD123+ PDCs was observed to be higher in OLE than OLP in the mucosal-submucosal junction (MSJ) (p = 0.021), the superficial perivascular area (p = 0.026), and the superficial and deep perivascular areas (p = 0.001). Likewise, PDCs in clusters ≥2+ were seen in significantly higher numbers on OLE than OLP along the MSJ (p = 0.002), the superficial perivascular area (p < 0.001), as well as the superficial and deep perivascular areas (p = 0.011). CD123+ PDCs were found to be significantly more numerous in both OLE and OLP than other OLLs in all of the abovementioned areas (all p < 0.05). Conclusion: While there are some differences in the clinicopathological features between OLE, OLP, as well as other OLLs, a significant overlap remains. The quantity and distribution pattern of CD123 immunohistochemical staining has a diagnostic implication in differentiating OLE from OLP and other OLLs.

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Diagnostic utility of plasmacytoid dendritic cells in dermatopathology

Cited by 7 publications

References 44 publications

Systemic lupus erythematosus patients contain B‐cell receptor repertoires sensitive to immunosuppressive drugs

Systemic lupus erythematosus patients contain B‐cell receptor repertoires sensitive to immunosuppressive drugs

Type 1 interferon signature and cytotoxic T lymphocyte activation targeted against sweat ducts in inflammatory acquired idiopathic generalized anhidrosis

Comparative Analyses of Clinical Features, Histopathology, and CD123 Immunohistochemistry of Oral Lupus Erythematosus, Lichen Planus, and Other Lichenoid Lesions

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