Oral Glucocorticoid–Sparing Effect of Benralizumab in Severe Asthma

Asthma is a common chronic inflammatory disease of the airways that affects an estimated 315 million persons worldwide. Approximately 5 to 10% of persons with asthma have a severe form of disease that is usually managed with high-dose inhaled glucocorticoids and bronchodilators. Within this group,…

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Oral Glucocorticoid–Sparing Effect of Benralizumab in Severe Asthma

Asthma is a common chronic inflammatory disease of the airways that affects an estimated 315 million persons worldwide. Approximately 5 to 10% of persons with asthma have a severe form of disease that is usually managed with high-dose inhaled glucocorticoids and bronchodilators. Within this group,…

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Oral Glucocorticoid–Sparing Effect of Benralizumab in Severe Asthma

Asthma is a common chronic inflammatory disease of the airways that affects an estimated 315 million persons worldwide. Approximately 5 to 10% of persons with asthma have a severe form of disease that is usually managed with high-dose inhaled glucocorticoids and bronchodilators. Within this group,…

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Monocyte-Derived Dendritic Cells: A Transendothelial Trip Launches the Quest To Understand Heterogeneity in the APC Family [PILLARS OF IMMUNOLOGY]

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Comment on "Diet-Derived Short Chain Fatty Acids Stimulate Intestinal Epithelial Cells To Induce Mucosal Tolerogenic Dendritic Cells" [LETTERS TO THE EDITOR]

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Determination of a Key Antigen for Immunological Intervention To Target the Latent Stage of Toxoplasma gondii [INFECTIOUS DISEASE AND HOST RESPONSE]

Toxoplasma gondii, an obligate intracellular protozoan parasite, establishes a chronic infection by forming cysts preferentially in the brain. Up to one third of the human population worldwide is estimated to be chronically infected with this parasite. However, there is currently no drug effective against the cyst form of the parasite. In addition, the protective immunity against the cysts remains largely unknown. We analyzed the molecular mechanisms by which the immune system detects host cells harboring the cysts to eliminate the latent stage of the parasite using mice with the H-2^d haplotype, which are genetically resistant to the infection. Our study revealed that CD8⁺ immune T cells bearing TCR Vβ8.1, 8.2 chain have a potent activity to remove T. gondii cysts from the brain. Our studies also uncovered that H-2L^d is the major Ag-presenting molecule to CD8⁺ T cells for initiating cyst elimination, and that CD8⁺Vβ8.1, 8.2⁺ immune T cells recognize the N-terminal region (aa 41–152) of dense granule protein 6 (GRA6Nt) of the parasite presented by the H-2L^d molecule. Furthermore, CD8⁺ immune T cells induced by immunization with recombinant GRA6Nt were eventually capable of removing the cysts from the brain when transferred to infected immunodeficient mice lacking T cells. Thus, GRA6Nt is a novel and potent Ag to activate CD8⁺ T cells capable of removing T. gondii cysts. These observations offer a basis for immunological intervention to combat chronic infection with T. gondii by targeting the persistent cysts of the parasite.

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IL-1R Type 1-Deficient Mice Demonstrate an Impaired Host Immune Response against Cutaneous Vaccinia Virus Infection [IMMUNE REGULATION]

The IL-1 superfamily of cytokines and receptors has been studied extensively. However, the specific roles of IL-1 elements in host immunity to cutaneous viral infection remain elusive. In this study, we applied vaccinia virus (VACV) by scarification to IL-1R1 knockout mice (IL-1R1^–/–) and found that these mice developed markedly larger lesions with higher viral genome copies in skin than did wild-type mice. The phenotype of infected IL-1R1^–/– mice was similar to eczema vaccinatum, a severe side effect of VACV vaccination that may develop in humans with atopic dermatitis. Interestingly, the impaired cutaneous response of IL-1R1^–/– mice did not reflect a systemic immune deficiency, because immunized IL-1R1^–/– mice survived subsequent lethal VACV intranasal challenge, or defects of T cell activation or T cell homing to the site of inoculation. Histologic evaluation revealed that VACV infection and replication after scarification were limited to the epidermal layer of wild-type mice, whereas lack of IL-1R1 permitted extension of VACV infection into dermal layers of the skin. We explored the etiology of this discrepancy and determined that IL-1R1^–/– mice contained significantly more macrophages and monocyte-derived dendritic cells in the dermis after VACV scarification. These cells were vulnerable to VACV infection and may augment the transmission of virus to adjacent skin, thus leading to larger skin lesions and satellite lesions in IL-1R1^–/– mice. These results suggest new therapeutic strategies for treatment of eczema vaccinatum and inform assessment of risks in patients receiving IL-1 blocking Abs for treatment of chronic inflammatory disorders.

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