Latest Articles Include:
- Antibody responses: Neutrophils zone in to help B cells | PDF (280 KB)
- Nat Rev Immunol 12(2):73 (2012)
Neutrophils are key effector cells of the innate immune system that are rapidly recruited to infected tissues to clear pathogens. Recently, researchers have shown that neutrophils also shape adaptive immune responses by interacting with T cells and dendritic cells (DCs). - Trafficking: Effector T cells cross the line | PDF (158 KB)
- Nat Rev Immunol 12(2):74 (2012)
Effector T cells migrate through the endothelial cell wall of blood vessels into inflamed tissues. Selectins, integrins and chemokine receptors have a central role in T cell extravasation, which involves the steps of cell arrest, spreading, crawling and transendothelial migration. - T cells: The TFH-like transition of TH1 cells | PDF (254 KB)
- Nat Rev Immunol 12(2):74 (2012)
The extent to which T helper (TH) cell subsets — including T follicular helper (TFH) cells — are distinct cell lineages has been the subject of much debate in recent years. Now, new evidence suggests that early during their development TH1 cells pass through a TH1–TFH cell stage, which involves a dynamic balance of signals mediated by the transcription factors signal transducer and activator of transcription 4 (STAT4), T-bet and B cell lymphoma 6 (BCL-6). - Mucosal immunology: Multifunctional gut IgA+ plasma cells | PDF (262 KB)
- Nat Rev Immunol 12(2):75 (2012)
The production of polyreactive IgA by plasma cells in the gastrointestinal tract is important for maintaining mucosal homeostasis. But do plasma cells in the intestine have functions that go beyond IgA production? - Viral immunity: Lose TRAF1, lose control | PDF (137 KB)
- Nat Rev Immunol 12(2):76 (2012)
Recent research describes a new defect that is associated with CD8+ T cell dysfunction in chronic viral infection. An acquired loss of expression of the signalling adaptor TNFR-associated factor 1 (TRAF1) from virus-specific CD8+ T cells during HIV infection in humans and during chronic lymphocytic choriomeningitis virus (LCMV) infection in mice decreases their ability to control the virus. - Immunometabolism: IL-15 provides breathing space for memory | PDF (269 KB)
- Nat Rev Immunol 12(2):76 (2012)
Memory T cells promote long-term resistance to infection, and uncovering the mechanisms that control their development and function is an important goal for immunologists. Van der Windt et al.+ T cells possess greater mitochondrial spare respiratory capacity (SRC) than naive or effector T cells. - Autoimmunity: Interfering with brain inflammation | PDF (161 KB)
- Nat Rev Immunol 12(2):77 (2012)
Interferon-β (IFNβ) is a first-line therapy for patients with relapsing–remitting multiple sclerosis. This study provides insight into the pathways by which type I IFNs can suppress inflammation in the central nervous system (CNS) and suggests a new mechanism by which these pathways could be targeted therapeutically. - Innate immunity: Phagocytes come back even stronger | PDF (112 KB)
- Nat Rev Immunol 12(2):74 (2012)
Lauvau and colleagues have shown that inflammatory monocytes and neutrophils become better pathogen killers during memory responses. The authors found that the enhanced clearance of the intracellular pathogen Listeria monocytogenes following re-infection was associated with increased reactive oxygen species (ROS)-mediated bacterial killing. -
- Nat Rev Immunol 12(2):74 (2012)
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- Nat Rev Immunol 12(2):74 (2012)
- Viral infection and the evolution of caspase 8-regulated apoptotic and necrotic death pathways
- Nat Rev Immunol 12(2):79 (2012)
Pathogens specifically target both the caspase 8-dependent apoptotic cell death pathway and the necrotic cell death pathway that is dependent on receptor-interacting protein 1 (RIP1; also known as RIPK1) and RIP3 (also known as RIPK3). The fundamental co-regulation of these two cell death pathways emerged when the midgestational death of mice deficient in FAS-associated death domain protein (FADD) or caspase 8 was reversed by elimination of RIP1 or RIP3, indicating a far more entwined relationship than previously appreciated. Thus, mammals require caspase 8 activity during embryogenesis to suppress the kinases RIP1 and RIP3 as part of the dialogue between two distinct cell death processes that together fulfil reinforcing roles in the host defence against intracellular pathogens such as herpesviruses. - How do plants achieve immunity? Defence without specialized immune cells
- Nat Rev Immunol 12(2):89 (2012)
Vertebrates have evolved a sophisticated adaptive immune system that relies on an almost infinite diversity of antigen receptors that are clonally expressed by specialized immune cells that roam the circulatory system. These immune cells provide vertebrates with extraordinary antigen-specific immune capacity and memory, while minimizing self-reactivity. Plants, however, lack specialized mobile immune cells. Instead, every plant cell is thought to be capable of launching an effective immune response. So how do plants achieve specific, self-tolerant immunity and establish immune memory? Recent developments point towards a multilayered plant innate immune system comprised of self-surveillance, systemic signalling and chromosomal changes that together establish effective immunity. - Transcriptional programming of the dendritic cell network
- Nat Rev Immunol 12(2):101 (2012)
Specialized subsets of dendritic cells (DCs) provide a crucial link between the innate and adaptive immune responses. The genetic programme that coordinates these distinct DC subsets is controlled by both cytokines and transcription factors. The initial steps in DC specification occur in the bone marrow and result in the generation of precursors committed to either the plasmacytoid or conventional DC pathways. DCs undergo further differentiation and lineage diversification in peripheral organs in response to local environmental cues. In this Review, we discuss new evidence regarding the coordination of the specification and commitment of precursor cells to different DC subsets and highlight the ensemble of transcription factors that control these processes. - Early immune events in the induction of allergic contact dermatitis
- Nat Rev Immunol 12(2):114 (2012)
The skin is a barrier site that is exposed to a wide variety of potential pathogens. As in other organs, pathogens that invade the skin are recognized by pattern-recognition receptors (PRRs). Recently, it has been recognized that PRRs are also engaged by chemical contact allergens and, in susceptible individuals, this elicits an inappropriate immune response that results in allergic contact dermatitis. In this Review, we focus on how contact allergens promote inflammation by activating the innate immune system. We also examine how innate immune cells in the skin, including mast cells and dendritic cells, cooperate with each other and with T cells and keratinocytes to initiate and drive early responses to contact allergens. - Immunomodulatory functions of type I interferons
- Nat Rev Immunol 12(2):125 (2012)
Interferon-α (IFNα) and IFNβ, collectively known as type I IFNs, are the major effector cytokines of the host immune response against viral infections. However, the production of type I IFNs is also induced in response to bacterial ligands of innate immune receptors and/or bacterial infections, indicating a broader physiological role for these cytokines in host defence and homeostasis than was originally assumed. The main focus of this Review is the underappreciated immunomodulatory functions of type I IFNs in health and disease. We discuss their function in the regulation of innate and adaptive immune responses, the response to bacterial ligands, inflammasome activation, intestinal homeostasis and inflammatory and autoimmune diseases. - Expanding roles for CD4+ T cells in immunity to viruses
- Nat Rev Immunol 12(2):136 (2012)
Viral pathogens often induce strong effector CD4+ T cell responses that are best known for their ability to help B cell and CD8+ T cell responses. However, recent studies have uncovered additional roles for CD4+ T cells, some of which are independent of other lymphocytes, and have described previously unappreciated functions for memory CD4+ T cells in immunity to viruses. Here, we review the full range of antiviral functions of CD4+ T cells, discussing the activities of these cells in helping other lymphocytes and in inducing innate immune responses, as well as their direct antiviral roles. We suggest that all of these functions of CD4+ T cells are integrated to provide highly effective immune protection against viral pathogens.
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