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Authorship note: S. Song and SD are co-first authors. Conflict of interest: BJB is an inventor on a US patent application (US20200071370A1, Cell-penetrating peptides that inhibit IRF5 nuclear localization), assigned to Rutgers. BJB and S. Sun are inventors on a US provisional patent application (62/844,894, Inhibition of IRF5 protects from lupus onset and severity), assigned to Feinstein Institutes.

Allergic asthma is a chronic respiratory disease that results from an exaggerated inflammatory response in the airways. Environment stimuli, such as pollen and HDM, cause activation and migration of inflammatory WBCs into the respiratory tract, where they cause lung damage. Migration of these WBCs is dependent on the active configuration of the β2 integrin LFA-1. The experimental therapeutic agent LtxA specifically targets active LFA-1 and causes cell death. We investigated the association between LFA-1 and allergic asthma and hypothesized that targeting LFA-1 with LtxA could be an attractive strategy for treatment of the condition. We examined LFA-1 (CD11a) levels on PBMCs from patients with allergic asthma compared with healthy controls. Patients exhibited a significantly higher percentage of PBMCs expressing LFA-1 than healthy controls. Furthermore, the level of LFA-1 expression on patient PBMCs was greater than on healthy PBMCs. We identified a unique cellular population in patients that consisted of CD4(-) CD11a(hi) cells. We also evaluated LtxA in a HDM extract-induced mouse model for allergic asthma. LtxA caused resolution of disease in mice, as demonstrated by a decrease in BALF WBCs, a reduction in pulmonary inflammation and tissue remodeling, and a decrease in proinflammatory cytokines IL-4, IL-5, IL-9, IL-17F, and IL-23α in lung tissue. LFA-1 may serve as an important marker in allergic asthma, and the elimination of activated WBCs by use of LtxA could be a viable therapeutic strategy for treating patients with this condition.

Immune hyperactivation has been linked to various vaccines. We present a potential association of newonset systemic lupus erythematosus (SLE) post-COVID-19 immunization. The patient is a 54-year-old male admitted for evaluation of flu-like symptoms two weeks after receiving the second dose of the COVID-19 vaccine. Physical examination revealed high-grade fever, diffuse bilateral non-tender cervical lymphadenopathy, and erythematous maculopapular palpable purpuric lesions on bilateral feet. Laboratory evaluation showed a significant hypocomplementemia (C3 < 11 mg/dL, C4 < 3 mg/dL, and CH50 < 10 U/mL), high titer antinuclear antibody, anti-dsDNA antibodies, anti-Sjogren's syndrome-related antigen A antibodies, anti-Sjogren's syndrome-related antigen B antibodies, anti-Smith antibodies, antiribonucleoprotein antibodies, anti-histone antibodies with a negative malignancy, and infection workup. The patient was treated with a high dose of steroids with a positive response. This case highlights the possibility of SLE, a rare adverse event following COVID-19 vaccination.

Mesenchymal stem cells (MSCs) are promising cellular suppressor of inflammation. This function of MSCs is partly due to their licensing by inflammatory mediators. In cases with reduced inflammation, MSCs could become immune-enhancer cells. MSCs can suppress the inflammatory response of antigen-challenged lymphocytes from allergic asthma. Although allergic rhinitis (AR) is also an inflammatory response, it is unclear if MSCs can exert similar suppression. This study investigated the immune effects (suppressor vs enhancer) of MSCs on allergen-stimulated lymphocytes from AR subjects (grass or weed allergy). In contrast to subjects with allergic asthma, MSCs caused a significant (P<0.05) increase in the proliferation of antigen-challenged lymphocytes from AR subjects. The increase in lymphocyte proliferation was caused by the MSCs presenting the allergens to CD4+ T cells (antigen-presenting cells (APCs)). This correlated with increased production of inflammatory cytokines from T cells, and increased expressions of major histocompatibility complex (MHC)-II and CD86 on MSCs. The specificity of APC function was demonstrated in APC assay using MSCs that were knocked down for the master regulator of MHC-II transcription, CIITA. The difference in the effects of MSCs on allergic asthma and AR could not be explained by the sensitivity to the allergen, based on skin tests. Thus, we deduced that the contrasting immune effects of MSCs for antigen-challenged lymphocytes on AR and allergic asthma could be disease specific. It is possible that the enhanced inflammation from asthma might be required to license the MSCs to become suppressor cells. This study underscores the need for robust preclinical studies to effectively translate MSCs for any inflammatory disorder.

We describe a 46-year-old male with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection who presented as a Kawasaki-like syndrome with features including prolonged fever, bilateral conjunctivitis, oral mucosal swelling, diffuse erythematous rash, cervical and hilar lymphadenopathy, as well as cardiovascular complications and multi-organ failure. There are several reports of a similar clinical entity mimicking Kawasaki disease (KD) in the pediatric population, which has been termed Pediatric Inflammatory Multisystem Syndrome Temporally Associated with SARS-CoV-2 (PIMS-TS) by the Royal College of Pediatric and Child Health. To our knowledge, to date, there has been only one case report of COVID-19 presenting as KD in an adult patient.

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Sarcoidosis is a granulomatous disease of unknown etiology that affects multiple organ systems. Neurological manifestations of sarcoidosis are less common and can include cranial neuropathies and intracranial lesions. We report the case of a 21-year-old man who presented with vertigo and uveitis. Extensive workup including brain imaging revealed enhancing focal lesions. A lacrimal gland biopsy confirmed the diagnosis of sarcoidosis. The patient was initially treated with prednisone, which did not adequately control his symptoms, and then was switched to methotrexate with moderate symptomatic improvement. Our patient had an atypical presentation with vertigo as the predominant manifestation of sarcoidosis. Patients with neurosarcoidosis typically present with systemic involvement of sarcoidosis followed by neurologic involvement. Vertigo is rarely reported as an initial manifestation. This case highlights the importance of consideration of neurosarcoidosis as an entity even in patients that may not have a typical presentation or systemic involvement of disease.