The autosomal recessive hyper-IgE syndrome (HIES) caused by dedicator of cytokinesis 8 (DOCK8) deficiency shares clinical features with autosomal dominant HIES because of signal transducer and activator of transcription 3 (STAT3) mutations, including recurrent infections and mucocutaneous candidiasis, which are suggestive of TH17 cell dysfunction. The mechanisms underlying this phenotypic overlap are unclear.

Autosomal dominant hyper-IgE syndrome caused by dominant-negative loss-of-function mutations in signal transducer and activator of transcription factor 3 (STAT3) (STAT3-HIES) is a rare primary immunodeficiency with multisystem pathology.

Although chronic urticaria (CU) is a common and primarily affects females, there is little data on how pregnancy interacts with the disease.

The recombination-activating gene (RAG) 1/2 proteins play a critical role in the development of T and B cells by initiating the VDJ recombination process that leads to generation of a broad T-cell receptor (TCR) and B-cell receptor repertoire. Pathogenic mutations in the RAG1/2 genes result in various forms of primary immunodeficiency, ranging from T(-)B(-) severe combined immune deficiency to delayed-onset disease with granuloma formation, autoimmunity, or both. It is not clear what contributes to such heterogeneity of phenotypes.

The authors evaluate major immunologic features of asthma and allergies in a Kuwaiti population. They analyzed peripheral venous blood from 17 asthmatic and 17 healthy long-term residents of Kuwait by using two-color flow cytometry for major lymphocyte subpopulations; they also evaluated 10 healthy individuals who had recently arrived in Kuwait.

Combined immunodeficiency with multiple intestinal atresias (CID-MIA) is a rare hereditary disease characterized by intestinal obstructions and profound immune defects.

Kuwait is a desert country where the prevailing high temperatures, low humidity, and scant vegetation suggest a low prevalence of allergy.

This study was designed to flow cytometrically determine baseline and sequential values of CD4 and CD8 lymphocyte subsets in patients without the human immunodeficiency virus and with pulmonary tuberculosis (TB) and to correlate these values with those obtained from normal male blood donors and with the radiologic extent of disease and response to therapy.

Patients with severe asthma may present with characteristics representing overlapping phenotypes, making them eligible for more than one class of biologic. Our aim was to describe the profile of adult patients with severe asthma eligible for both anti-IgE and anti-IL5/5R and to compare the effectiveness of both classes of treatment in real life.

There is an increased demand for hematopoietic stem cell transplant (HSCT) to treat various diseases including combined immunodeficiencies (CID), with limited worldwide availability. Variables affecting the decision regarding CID patients' prioritization for HSCT are not known. We aimed to determine general, clinical, and immunologic factors associated with the higher risk of early death (≤6 months after diagnosis) in untransplanted CID patients.

A history of nonsteroidal anti-inflammatory drug (NSAID) hypersensitivity with cross-intolerance to several drugs is common in some patients with coronary artery disease. We present a series of patients with acute coronary syndrome undergoing ASA desensitization prior to a possible stent to evaluate the short- and long-term efficacy and safety. The aim was to evaluate the outcomes of an ASA desensitization protocol developed by our center based on the guidelines proposed by the EAACI drug allergy expert recommendations.

The DNA segments corresponding to two members of the mammalian cell entry operon 1 (mce1) encoding Mce1A and Mce1E proteins were amplified from Mycobacterium tuberculosis genomic DNA by polymerase chain reaction, cloned and subcloned into pGEM-T and pGEX-4T-3 vectors, respectively, and expressed in Escherichia coli as fusion proteins with glutathione-S-transferase (GST) of Schistosoma japonicum as the fusion partner.