Publications by authors named "Alicia J Little"

10 Publications

  • Page 1 of 1

Post-COVID-19 vaccination IgA Vasculitis in an Adult.

J Cutan Pathol 2021 Nov 14. Epub 2021 Nov 14.

Department of Dematology, Yale University School of Medicine.

Leukocytoclastic vasculitis has been reported in the setting of COVID-19 infection and post-COVID-19 vaccination. We report a case of post-COVID-19 vaccination IgA vasculitis with IgA immune deposits in the skin and renal involvement; SARS-CoV spike protein immunohistochemical staining was negative. IgA vasculitis with skin and renal involvement is a potential reaction to COVID-19 vaccination. This article is protected by copyright. All rights reserved.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/cup.14168DOI Listing
November 2021

Delayed Localized Hypersensitivity Reactions to the Moderna COVID-19 Vaccine: A Case Series.

JAMA Dermatol 2021 06;157(6):716-720

Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut.

Importance: In response to the coronavirus disease 2019 (COVID-19) pandemic, 2 mRNA vaccines (Pfizer-BioNTech and Moderna) received emergency use authorization from the US Food and Drug Administration in December 2020. Some patients in the US have developed delayed localized cutaneous vaccine reactions that have been dubbed "COVID arm."

Objective: To describe the course of localized cutaneous injection-site reactions to the Moderna COVID-19 vaccine, subsequent reactions to the second vaccine dose, and to characterize the findings of histopathologic examination of the reaction.

Design, Setting, And Participants: This retrospective case series study was performed at Yale New Haven Hospital, a tertiary medical center in New Haven, Connecticut, with 16 patients referred with localized cutaneous injection-site reactions from January 20 through February 12, 2021.

Main Outcomes And Measures: We collected each patient's demographic information, a brief relevant medical history, clinical course, and treatment (if any); and considered the findings of a histopathologic examination of 1 skin biopsy specimen.

Results: Of 16 patients (median [range] age, 38 [25-89] years; 13 [81%] women), 14 patients self-identified as White and 2 as Asian. The delayed localized cutaneous reactions developed in a median (range) of 7 (2-12) days after receiving the Moderna COVID-19 vaccine. These reactions occurred at or near the injection site and were described as pruritic, painful, and edematous pink plaques. None of the participants had received the Pfizer-BioNTech vaccine. Results of a skin biopsy specimen demonstrated a mild predominantly perivascular mixed infiltrate with lymphocytes and eosinophils, consistent with a dermal hypersensitivity reaction. Of participants who had a reaction to first vaccine dose (15 of 16 patients), most (11 patients) developed a similar localized injection-site reaction to the second vaccine dose; most (10 patients) also developed the second reaction sooner as compared with the first-dose reaction.

Conclusions And Relevance: Clinical and histopathologic findings of this case series study indicate that the localized injection-site reactions to the Moderna COVID-19 vaccine are a delayed hypersensitivity reaction. These reactions may occur sooner after the second dose, but they are self-limited and not associated with serious vaccine adverse effects. In contrast to immediate hypersensitivity reactions (eg, anaphylaxis, urticaria), these delayed reactions (dubbed "COVID arm") are not a contraindication to subsequent vaccination.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1001/jamadermatol.2021.1214DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8117061PMC
June 2021

Epidermolysis bullosa pruriginosa treated with dupilumab.

Pediatr Dermatol 2021 Mar 18;38(2):526-527. Epub 2020 Dec 18.

Department of Dermatology, Yale University School of Medicine, New Haven, CT, USA.

Epidermolysis bullosa pruriginosa (EBP) is a variant of dystrophic epidermolysis bullosa characterized by intense pruritus and prurigo nodularis-like lesions. While medical therapies for EBP exist, current treatments are not consistently effective, and symptoms often cause decreased quality of life. Here, we report two cases of EBP treated with dupilumab, which decreased symptoms of pruritus and improved skin findings. Both patients have been on dupilumab for over one year with sustained improvement and no adverse effects; although in one patient, increased dosing was required to attain optimal control of disease.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/pde.14493DOI Listing
March 2021

Erythema nodosum due to infection complicating autologous fat transfer.

Int J Womens Dermatol 2020 Sep 27;6(4):340-341. Epub 2020 May 27.

Department of Dermatology, Yale School of Medicine, New Haven, CT, United States.

View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.ijwd.2020.05.011DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7522915PMC
September 2020

Cutaneous Lupus Erythematosus: Current and Future Pathogenesis-Directed Therapies.

Yale J Biol Med 2020 03 27;93(1):81-95. Epub 2020 Mar 27.

Department of Dermatology, Yale School of Medicine, New Haven, CT.

Cutaneous lupus erythematosus (CLE) is an autoimmune disease of the skin with significant morbidity. Current treatments are often inadequate to control disease and there are no Food and Drug Administration (FDA)-approved therapies for this potentially debilitating disease, underscoring an unmet medical need. Recent insights into disease pathogenesis have implicated innate and adaptive immune components, including type I and type III interferons in the development of CLE. Promising clinical trials based on these insights are now underway. However, the full spectrum of immune cells, cytokines, and environmental triggers contributing to disease remain to be elucidated. In this review, we will highlight the current understanding of CLE immunopathogenesis, the ongoing clinical trial landscape, and provide a framework for designing future therapeutic strategies for CLE based on new insights into disease pathogenesis.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7087060PMC
March 2020

Rapidly enlarging nodular plaque on the leg.

JAMA Dermatol 2014 Oct;150(10):1107-8

Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut.

View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1001/jamadermatol.2014.1045DOI Listing
October 2014

Cooperative recruitment of HMGB1 during V(D)J recombination through interactions with RAG1 and DNA.

Nucleic Acids Res 2013 Mar 15;41(5):3289-301. Epub 2013 Jan 15.

Department of Immunobiology, Yale University School of Medicine, 300 Cedar Street, New Haven, CT 06511, USA.

During V(D)J recombination, recombination activating gene (RAG)1 and RAG2 bind and cleave recombination signal sequences (RSSs), aided by the ubiquitous DNA-binding/-bending proteins high-mobility group box protein (HMGB)1 or HMGB2. HMGB1/2 play a critical, although poorly understood, role in vitro in the assembly of functional RAG-RSS complexes, into which HMGB1/2 stably incorporate. The mechanism of HMGB1/2 recruitment is unknown, although an interaction with RAG1 has been suggested. Here, we report data demonstrating only a weak HMGB1-RAG1 interaction in the absence of DNA in several assays, including fluorescence anisotropy experiments using a novel Alexa488-labeled HMGB1 protein. Addition of DNA to RAG1 and HMGB1 in fluorescence anisotropy experiments, however, results in a substantial increase in complex formation, indicating a synergistic binding effect. Pulldown experiments confirmed these results, as HMGB1 was recruited to a RAG1-DNA complex in a RAG1 concentration-dependent manner and, interestingly, without strict RSS sequence specificity. Our finding that HMGB1 binds more tightly to a RAG1-DNA complex over RAG1 or DNA alone provides an explanation for the stable integration of this typically transient architectural protein in the V(D)J recombinase complex throughout recombination. These findings also have implications for the order of events during RAG-DNA complex assembly and for the stabilization of sequence-specific and non-specific RAG1-DNA interactions.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1093/nar/gks1461DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3597659PMC
March 2013

Promoters, enhancers, and transcription target RAG1 binding during V(D)J recombination.

J Exp Med 2010 Dec 29;207(13):2809-16. Epub 2010 Nov 29.

Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.

V(D)J recombination assembles antigen receptor genes in a well-defined order during lymphocyte development. This sequential process has long been understood in the context of the accessibility model, which states that V(D)J recombination is regulated by controlling the ability of the recombination machinery to gain access to its chromosomal substrates. Indeed, many features of "open" chromatin correlate with V(D)J recombination, and promoters and enhancers have been strongly implicated in creating a recombinase-accessible configuration in neighboring chromatin. An important prediction of the accessibility model is that cis-elements and transcription control binding of the recombination-activating gene 1 (RAG1) and RAG2 proteins to their DNA targets. However, this prediction has not been tested directly. In this study, we use mutant Tcra and Tcrb alleles to demonstrate that enhancers control RAG1 binding globally at Jα or Dβ/Jβ gene segments, that promoters and transcription direct RAG1 binding locally, and that RAG1 binding can be targeted in the absence of RAG2. These findings reveal important features of the genetic mechanisms that regulate RAG binding and provide a direct confirmation of the accessibility model.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1084/jem.20101136DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3005232PMC
December 2010
-->