The rapid development and the launch of several novel COVID-19 vaccines for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an extraordinary and remarkable accomplishment of modern science. The Pfizer-BioNTech BNT162b2 was the first vaccine to be granted temporary authorization for emergency use by the Medicines and Healthcare Products Regulatory Agency (MHRA) in the U.K for the treatment of COVID-19 on 2 December 2020. 1 Soon after, on 11 December 2020, it also received emergency use authorization (EUA) by the U.S. Food and Drug Administration (FDA). 2 EUA is a mechanism to facilitate the availability of vaccines during public health emergencies, such as the current COVID-19 pandemic. Under an EUA, the FDA may allow the use of unapproved medical products (including vaccines) to prevent serious or life-threatening disease when certain statutory criteria have been met and no adequate and/or approved alternatives are available. The authorization of BNT162b2 was followed by an EUA for a second COVID-19 vaccine, the Moderna mRNA-1273 on 18 December 2020. 3 This was followed by the authorization of mRNA-1273 for use by other regulatory agencies such as the European Commission, UK MHRA, Israel Ministry of

Vaccines are essential public health tools with a favorable safety profile and prophylactic effectiveness that have historically played significant roles in reducing infectious disease burden in populations, when the majority of individuals are vaccinated. The COVID-19 vaccines are expected to have similar positive impacts on health across the globe. While serious allergic reactions to vaccines are rare, their underlying mechanisms and implications for clinical management should be considered to provide individuals with the safest care possible. In this review, we provide an overview of different types of allergic adverse reactions that can potentially occur after vaccination and individual vaccine components capable of causing the allergic adverse reactions. We present the incidence of allergic adverse reactions during clinical studies and through post-authorization and post-marketing surveillance and provide plausible causes of these reactions based on potential allergenic components present in several common vaccines. Additionally, we review implications for individual diagnosis and management and vaccine manufacturing overall. Finally, we suggest areas for future research.

Background The incidence of adult‐onset atopic dermatitis (AOAD) is increasing. However, the unique characteristics of AOAD compared to pediatric‐onset AD persisting into adulthood (POAD) are underexplored, hampering the development of targeted‐therapeutics for this growing population. We thus assessed the profile of AOAD in skin and blood compared to that of POAD. Methods We collected skin biopsies and blood from adults with AOAD, POAD, and healthy controls (n = 15 in each group). Skin samples were analyzed by RNA sequencing, qRT‐PCR, and immunohistochemistry, and Olink Proseek multiplex assay was used to identify the serum proteomic profile. Results Compared to healthy controls, both AOAD and POAD showed cutaneous immune and barrier dysregulations with a shared Th2/Th22 hyperactivation. Overall, POAD showed greater inflammation in lesional skin, with more prominent expression of Th2/Th17/Th22 markers (CCL17/22, S100A8/9, IL‐36A, PI3/Elafin, DEFB4) in POAD compared to AOAD (p‐value < .05). In contrast, higher Th1‐(IFN‐γ, IL‐2, IL‐15, CCL5) upregulation and Th1‐skewing were seen in AOAD. The epidermal barrier was also more compromised in POAD, with greater epidermal hyperplasia and lower expression of markers related to terminal differentiation, lipids, and cell adhesion. In parallel with increased rates of cardiovascular comorbidities, AOAD demonstrated many more significantly dysregulated proteins in serum (n = 148) compared to POAD (n = 86), including pro‐inflammatory and cardiovascular‐risk markers. Th1‐related products showed significant correlations between their skin and blood expressions only in AOAD subjects. Conclusion Age‐of‐onset delineates two distinct endophenotypes in adult AD potentially suggesting the need for broader (beyond Th2) therapeutic targeting in AOAD.

No abstract

No abstract