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    ON THE COVER
    Recent papers from Cha et al. (this issue) and Zenonos et al. (July 27 issue) identify cellular targets to block malaria parasite invasion by inhibiting access to the liver via a Kupffer cell receptor and host red blood cell receptors, respectively. Illustration by Emilie Clark (Emilie@emilieclark.com).
    See page 1391

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ISSN 0022-1007
EISSN 1540-9538
In this Issue

Insights

Review

Buck et al. discuss the role of lymphocyte metabolism on immune cell development and function.

Bournazos, DiLillo, and Ravetch discuss the biology of Fc receptors and their contribution to the effector function of protective antibody responses during infections and in therapeutics.

Brief Definitive Report

Andersen et al. identify a novel genetic etiology of herpes encephalitis in an adult patient carrying a heterozygous loss-of-function mutation in the IRF3 gene. This mutation results in impaired INF production in response to viral infection

Lee et al. find that phospholipase D2 deficiency increases survival and decreases organ damage during experimental sepsis in mice which could be reversed with a CXCR2 antagonist. Thus, targeting PLD2 may offer therapeutics for septic patients.

Article

Cha et al. use a phage display library screen to identify a peptide, P39, that binds to CD68 on the surface of Kupffer cells to inhibit malaria sporozoite cell entry. Thus, P39 may represent a therapeutic strategy for malaria by limiting hepatic infection.

While people infected with Leishmania can become refractory to reinfection, human vaccines have not yet been achieved. Glennie et al. identify a population of skin-resident Leishmania-specific memory T cells that produce IFN-γ and recruit circulating T cells to the skin in response to a subsequent parasitic infection. The findings indicate that a successful vaccine may be dependent on generating skin-resident memory T cells for an effective immune response.

Ruppert et al. report that Kindlin-3–mediated integrin activation controls homing of hematopoietic stem cells (HSCs) to the bone marrow (BM) and the retention of activated, but not quiescent, HSCs in the BM niche.

Qian et al. show that the receptor tyrosine kinase FLT1 is highly expressed in a subset of macrophages enriched in breast cancer metastatic sites. Inhibition of this kinase reduces metastasis to the lungs by blocking signaling via focal adhesion kinase 1 to an inflammatory state in the macrophages centered on signaling from the macrophage growth factor, colony stimulating factor-1.

Loss of IL-27R on T cells results in increased protection from Mycobacterium tuberculosis. Torrado et al. demonstrate that IL-27R−/− T cells show improved fitness that is associated with decreased expression of cell death molecules, maintenance of IL-2 production, and preferential accumulation in the lung parenchyma and around infected macrophages.

Inoue et al. report that CNOT3, a subunit of the CCR4–NOT deadenylase complex regulating mRNA decay and translational repression, controls Igh gene rearrangement and destabilizes the mRNA of the tumor suppressor p53. Loss of CNOT3 results in a block of pro- to pre–B cell transition.

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