Infection and Immunity最新文献

{"title":"Polycytotoxic T cells mediate antimicrobial activity against intracellular <i>Mycobacterium tuberculosis</i>.","authors":"Marc Zumwinkel, Aaron Chirambo, Markus Zähnle, Max Bürger, Mark Grieshober, Vincent Romahn, Henry Mwandumba, Steffen Stenger","doi":"10.1128/iai.00297-24","DOIUrl":"10.1128/iai.00297-24","url":null,"abstract":"<p><p>Protection against infections with intracellular bacteria requires the interaction of macrophages and T-lymphocytes, including CD8⁺ T cells. Recently, the expression of natural killer cell receptors NKG2A and NKG2C was introduced as markers of CD8⁺ T-cell subsets. The goal of this study was to functionally characterize human NKG2A and NKG2C-expressing T cells using the major pathogen <i>Mycobacterium tuberculosis</i> (<i>Mtb</i>) as a model organism. Sorted NKG2 populations were analyzed for their capacity to proliferate and degranulate and their intracellular expression of cytotoxic molecules. Cytokine release and the effect on bacterial growth were assessed after coculture of NKG2 populations with <i>Mtb</i>-infected macrophages. NKG2A⁺ T cells released higher levels of IFN-γ and IL-10, whereas NKG2C⁺ T cells released higher levels of IL-2, contained the greatest reservoir of intracellular granzyme B and showed a remarkable constitutive level of degranulation. Both subsets inhibited the intracellular growth of <i>Mtb</i> more efficiently than NKG2-negative CD8⁺ T cells. Antimicrobial activity of NKG2⁺ T cells was not associated with the release of cytokines or cytotoxic molecules. However, the frequency of polycytotoxic T cells (P-CTL), defined as CD8⁺ T cells co-expressing granzyme B, perforin, and granulysin, positively correlated with the ability of NKG2-expressing T cells to control <i>Mtb</i>-growth in macrophages. Our results highlight the potential of NKG2-expressing P-CTL to trigger the antibacterial activity of human macrophages. Targeting this population by preventive or therapeutic immune interventions could provide a novel strategy to combat severe infectious diseases such as tuberculosis.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0029724"},"PeriodicalIF":2.9,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11784352/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Infection-induced trained immunity: a twist in paradigm of innate host defense and generation of immunological memory.","authors":"Aayush Bahl, Saurabh Pandey, Roopshali Rakshit, Sashi Kant, Deeksha Tripathi","doi":"10.1128/iai.00472-24","DOIUrl":"10.1128/iai.00472-24","url":null,"abstract":"<p><p>In contrast to adaptive immunity, which relies on memory T and B cells for long-term pathogen-specific responses, trained immunity involves the enhancement of innate immune responses through cellular reprogramming. Experimental evidence from animal models and human studies supports the concept of trained immunity and its potential therapeutic applications in the development of personalized medicine. However, there remains a huge gap in understanding the mechanisms, identifying specific microbial triggers responsible for the induction of trained immunity. This underscores the importance of investigating the potential role of trained immunity in redefining host defense and highlights future research directions. This minireview will provide a comprehensive summary of the new paradigm of trained immunity or innate memory pathways. It will shed light on infection-induced pathways through non-specific stimulation within macrophages and natural killer cells, which will be further elaborated in multiple disease perspectives caused by infectious agents such as bacteria, fungi, and viruses. The article further elaborates on the biochemical and cellular basis of trained immunity and its impact on disease status during recurrent exposures. The review concludes with a perspective segment discussing potential therapeutic benefits, limitations, and future challenges in this area of study. The review also sheds light upon potential risks involved in the induction of trained immunity.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0047224"},"PeriodicalIF":2.9,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11784091/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The ability of <i>sarA</i> to limit protease production plays a key role in the pathogenesis of <i>Staphylococcus aureus</i> osteomyelitis irrespective of the functional status of <i>agr</i>.","authors":"Karen E Beenken, Mara J Campbell, Mark S Smeltzer","doi":"10.1128/iai.00473-24","DOIUrl":"10.1128/iai.00473-24","url":null,"abstract":"&lt;p&gt;&lt;p&gt;We demonstrate that mutation of the staphylococcal accessory regulator A (&lt;i&gt;sarA&lt;/i&gt;) in the USA300 strain LAC limits virulence in a murine osteomyelitis model to a greater extent than mutation of the accessory gene regulator (&lt;i&gt;agr&lt;/i&gt;) and that it does so irrespective of the functional status of &lt;i&gt;agr&lt;/i&gt;. Protease production was decreased in the &lt;i&gt;agr&lt;/i&gt; mutant but increased in &lt;i&gt;sarA&lt;/i&gt; and &lt;i&gt;sarA/agr&lt;/i&gt; mutants to a degree that limited biofilm formation. Extracellular protein A (eSpa) and full-length extracellular nuclease (Nuc1) were absent in the conditioned medium (CM) from &lt;i&gt;sarA&lt;/i&gt; and &lt;i&gt;sarA&lt;/i&gt;/&lt;i&gt;agr&lt;/i&gt; mutants, and their abundance was restored in both mutants by eliminating protease production. Cytotoxicity of CM for osteoblasts and osteoclasts was also reduced in both mutants. Cytotoxicity was restored in a protease-deficient &lt;i&gt;sarA&lt;/i&gt; mutant but not in the protease-deficient &lt;i&gt;sarA&lt;/i&gt;/&lt;i&gt;agr&lt;/i&gt; mutant. Reduced cytotoxicity was correlated with the reduced abundance of full-length α-toxin, LukF, and LukS in &lt;i&gt;sarA&lt;/i&gt; and &lt;i&gt;sarA&lt;/i&gt;/&lt;i&gt;agr&lt;/i&gt; mutants. The abundance of these toxins in their full-length form was increased in the protease-deficient &lt;i&gt;sarA&lt;/i&gt; mutant by comparison to LAC, demonstrating that mutation of &lt;i&gt;sarA&lt;/i&gt; increases the production of these toxins but increased protease production limits their abundance in full-length and presumably functional forms. Most importantly, eliminating protease production enhanced the virulence of &lt;i&gt;sarA&lt;/i&gt; and &lt;i&gt;sarA/agr&lt;/i&gt; mutants, but had no impact in the &lt;i&gt;agr&lt;/i&gt; mutant. We conclude that a key factor in the attenuation of LAC &lt;i&gt;sarA&lt;/i&gt; and &lt;i&gt;sarA&lt;/i&gt;/&lt;i&gt;agr&lt;/i&gt; mutants in osteomyelitis is the increased production of extracellular proteases and its impact on virulence factors that contribute to biofilm formation and cytotoxicity.&lt;b&gt;IMPORTANCE&lt;/b&gt;The persistent emergence of antibiotic-resistant strains has rekindled interest in anti-virulence strategies to combat &lt;i&gt;S. aureus&lt;/i&gt; infections. Numerous reports describe anti-virulence strategies focusing on key regulatory elements that globally influence virulence factor production, the two most commonly targeted being the accessory gene regulator (&lt;i&gt;agr&lt;/i&gt;) and the staphylococcal accessory regulator A (&lt;i&gt;sarA&lt;/i&gt;). We demonstrate that mutation of &lt;i&gt;sarA&lt;/i&gt; limits virulence to a greater extent than mutation of &lt;i&gt;agr&lt;/i&gt; and that this can be attributed to increased protease production in both &lt;i&gt;sarA&lt;/i&gt; and &lt;i&gt;sarA&lt;/i&gt;/&lt;i&gt;agr&lt;/i&gt; mutants. This illustrates the critical role of &lt;i&gt;sarA&lt;/i&gt; in protease-mediated post-translational regulation in &lt;i&gt;S. aureus&lt;/i&gt;. It also suggests that an inhibitor of &lt;i&gt;sarA&lt;/i&gt; would be more effective than an inhibitor of &lt;i&gt;agr&lt;/i&gt; in overcoming the therapeutic recalcitrance of osteomyelitis and that such an inhibitor would remain effective even in the context of &lt;i&gt;agr&lt;/i&gt; mutants known to arise &lt;i&gt;in vivo&lt;/i&gt; during the transition from acute to chronic infection","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0047324"},"PeriodicalIF":2.9,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11784413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of Concern for Galdiero et al., \"<i>Haemophilus influenzae</i> Porin Contributes to Signaling of the Inflammatory Cascade in Rat Brain\".","authors":"","doi":"10.1128/iai.00490-24","DOIUrl":"10.1128/iai.00490-24","url":null,"abstract":"","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0049024"},"PeriodicalIF":2.9,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11784363/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Establishment of CD1b-restricted immunity to lipid antigens in the pulmonary response to <i>Mycobacterium tuberculosis</i> infection.","authors":"Macallister C Harris, Hadley E Gary, Sarah K Cooper, David F Ackart, James E DiLisio, Randall J Basaraba, Tan-Yun Cheng, Ildiko van Rhijn, D Branch Moody, Brendan K Podell","doi":"10.1128/iai.00380-24","DOIUrl":"10.1128/iai.00380-24","url":null,"abstract":"<p><p>CD1 is an antigen-presenting glycoprotein homologous to MHC I; however, CD1 proteins present lipid rather than peptide antigens. CD1 proteins are well established to present lipid antigens of <i>Mycobacterium tuberculosis</i> (Mtb) to T cells, but understanding the role of CD1-restricted immunity <i>in vivo</i> in response to Mtb infection has been limited by the availability of animal models naturally expressing the CD1 proteins implicated in human response: CD1a, CD1b, and CD1c. Guinea pigs, in contrast to other rodent models, express four CD1b orthologs, and here we utilize the guinea pig to establish the kinetics of gene and protein expression of CD1b orthologs, as well as the Mtb lipid-antigen and CD1b-restricted immune response at the tissue level over the course of Mtb infection. Our results indicate transient upregulation of CD1b expression during the effector phase of adaptive immunity that wanes with disease chronicity. Gene expression indicates that the upregulation of CD1b is the result of transcriptional induction across all CD1b orthologs. We show high CD1b3 expression on B cells, and identify CD1b3 as the predominant CD1b ortholog in pulmonary granuloma lesions. We identify <i>ex vivo</i> cytotoxic activity directed against CD1b that parallels the kinetic changes in CD1b expression in Mtb-infected lungs and spleen. This study confirms that CD1b expression is modulated by Mtb infection in lung and spleen, leading to pulmonary and extrapulmonary CD1b-restricted immunity as a component of the antigen-specific response to Mtb infection.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0038024"},"PeriodicalIF":2.9,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142568336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gene expression profiling reveals host defense strategies for restricting <i>Candida albicans</i> invasion and gastritis to the limiting ridge of the murine stomach.","authors":"Karen D Zeise, Nicole R Falkowski, Joseph D Metcalf, Christopher A Brown, Gary B Huffnagle","doi":"10.1128/iai.00438-24","DOIUrl":"10.1128/iai.00438-24","url":null,"abstract":"<p><p><i>Candida albicans</i> is a fungal constituent of the human gastrointestinal microbiota that can tolerate acidic environments like the stomach, where it can be associated with ulcers and chronic gastritis. In mice, <i>C. albicans</i> induces gastritis without concurrent intestinal inflammation, suggesting that the stomach is particularly prone to fungal infection. We previously showed that <i>C. albicans</i> invasion in the limiting ridge does not extend to or elicit an inflammatory response in the adjacent glandular region, indicating regionalized gastritis in the murine stomach. However, the molecular pathways involved in the host response to <i>C. albicans</i> specifically in the limiting ridge have not been investigated. Here, we found that gastric dysbiosis was associated with <i>C. albicans</i> limiting ridge colonization and gastritis. We isolated the limiting ridge and evaluated the expression of over 90 genes involved in mucosal responses. <i>C. albicans</i> infection triggered a type 3 immune response marked by elevated <i>Il17a</i>, <i>Il17f</i>, <i>Il1b</i>, <i>Tnf</i>, and <i>Il36g</i>, as well as an upregulation of <i>Il12a</i>, <i>Il4</i>, <i>Il10</i>, and <i>l13</i>. Chemokine gene induction (including <i>Ccl2</i>, <i>Ccl3</i>, <i>Ccl4</i>, <i>Ccl1l</i>, <i>Cxcl1</i>, <i>Cxcl2</i>, <i>Cxcl9</i>, and <i>Cxcl10</i>) coincided with an influx of neutrophils, monocytes/macrophages, and eosinophils. Hyphal invasion caused tissue damage, epithelial remodeling, and upregulation of genes linked to epithelium signaling and antimicrobial responses in the limiting ridge. Our findings support a need for continued exploration into the interactions between the immunological milieu, the host microbiota, and clinical interventions such as the use of antibiotics and immunotherapeutic agents and their collective impact on invasive candidiasis risk.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0043824"},"PeriodicalIF":2.9,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629626/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A conserved interaction between the effector Sca4 and host clathrin suggests additional contributions for Sca4 during rickettsial infection.","authors":"Cassandra J Vondrak, Brandon Sit, Chanakan Suwanbongkot, Kevin R Macaluso, Rebecca L Lamason","doi":"10.1128/iai.00267-24","DOIUrl":"10.1128/iai.00267-24","url":null,"abstract":"<p><p>Intracellular bacterial pathogens deploy secreted effector proteins that manipulate diverse host machinery and pathways to promote infection. Although many effectors carry out a single function or interaction, there are a growing number of secreted effectors capable of interacting with multiple host factors. However, few effectors secreted by arthropod-borne obligate intracellular <i>Rickettsia</i> species have been linked to multiple host targets. Here, we investigated the conserved rickettsial secreted effector Sca4, which was previously shown to interact with host vinculin in donor cells to promote cell-to-cell spread in the model <i>Rickettsia</i> species <i>R. parkeri</i>. We discovered that Sca4 also binds the host cell protein clathrin heavy chain (CHC, <i>CLTC</i>) via a conserved segment in the Sca4 N-terminus. In mammalian host cells, ablation of <i>CLTC</i> expression or chemical inhibition of endocytosis reduced <i>R. parkeri</i> cell-to-cell spread<i>,</i> indicating that clathrin promotes efficient spread. Unexpectedly, the contribution of CHC to spread was independent of Sca4 and appeared restricted to the recipient host cell, suggesting that the Sca4-clathrin interaction regulates another aspect of the infectious lifecycle. Indeed, <i>R. parkeri</i> lacking Sca4 or expressing a Sca4 truncation unable to bind clathrin had markedly reduced burdens in tick cells, hinting at a cell type-specific function for the Sca4-clathrin interaction. Sca4 homologs from diverse <i>Rickettsia</i> species also bound clathrin, suggesting that the function of this novel effector-host interaction may be broadly important for rickettsial infection. We conclude that Sca4 has multiple targets during infection and that rickettsiae may manipulate host endocytic machinery to facilitate several stages of their life cycles.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0026724"},"PeriodicalIF":2.9,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629629/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tail-specific protease is an essential <i>Chlamydia</i> virulence factor that mediates the differentiation of elementary bodies into reticulate bodies.","authors":"Arkaprabha Banerjee, Kaylee R Jacobs, Yihui Wang, Emma H Doud, Evelyn Toh, Barry D Stein, Amber L Mosley, Guangming Zhong, Richard P Morrison, Sandra G Morrison, Shuai Hu, Julie A Brothwell, David E Nelson","doi":"10.1128/iai.00436-24","DOIUrl":"10.1128/iai.00436-24","url":null,"abstract":"<p><p>Tail-specific proteases (Tsp) are members of a widely distributed family of serine proteases that commonly target and process periplasmic proteins in Gram-negative bacteria. The obligately intracellular, Gram-negative <i>Chlamydia</i> encode a highly conserved Tsp homolog whose target and function are unclear. We identified a <i>Chlamydia muridarum</i> mutant with a nonsense mutation in <i>tsp</i>. Differentiation of the <i>tsp</i> mutant elementary bodies into vegetative reticulate bodies was delayed at 37°C and completely blocked at 40°C. Tsp localized to <i>C. muridarum</i> cells but was not detected outside the inclusion, suggesting that it targets chlamydial rather than host proteins. The abundance of key chlamydia outer membrane complex and virulence-related proteins differed in wild-type and <i>tsp</i> mutant elementary bodies, consistent with the possibility that Tsp regulates developmental cycle progression. The altered abundances of chlamydial structural and virulence factors could explain why the mutant, but not an isogenic recombinant with wild-type <i>tsp</i>, was highly attenuated in a mouse intravaginal infection model. Thus, chlamydial Tsp is required for timely differentiation of elementary bodies into reticulate bodies <i>in vitro</i> and is an essential virulence factor <i>in vivo</i>.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0043624"},"PeriodicalIF":2.9,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629628/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential murine responses to <i>Schistosoma mansoni</i> eggs in the liver and small intestine lead to downmodulation of hepatic but not intestinal periovular granulomas.","authors":"Ashgan Montasser, Ahmad E Dakrory, Mohamed I M Ibrahim, Emad El Zayyat, Hatem Tallima, Rashika El Ridi","doi":"10.1128/iai.00362-24","DOIUrl":"10.1128/iai.00362-24","url":null,"abstract":"<p><p>To control schistosomiasis mansoni, it is important to attempt preventing the worms' egg-induced pathology in the liver and limiting pathogen transmission following egg exit from the intestines to the exterior. Therefore, the present study aimed to clarify the reasons behind the decades-long riddle of periovular granulomas downmodulation in the liver, but not the small intestine, with the progression of murine schistosomiasis mansoni. Outbred female CD-1 mice were percutaneously exposed to 15 <i>Schistosoma mansoni</i> cercariae. The liver and small intestine were collected from mice harboring a minimum of a worm couple at 8, 12, 16, and 20 weeks post-infection, assessed for egg counts/g and histopathological changes, and used to prepare Triton X-100 extracts. Content of cytokines, saturated and unsaturated fatty acids, triglycerides, cholesterol, reactive oxygen species, and uric acid per mg tissue extract proteins were evaluated using capture enzyme-linked immunosorbent assays, gas chromatography-flame ionization detector, and standard commercially available reagents, respectively. Examination of hematoxylin-eosin-stained tissue sections confirmed the decrease in size and changes in cellular composition of periovular granulomas in the liver but not the small intestine, associated with wide differences in released cytokines types and amounts, and content of the bioactive lipids, arachidonic and docosahexaenoic acids, reactive oxygen species, and uric acid. The results together disclosed that the downmodulation of hepatic, but not the small intestine, circumoval granulomas with the progression of murine <i>S. mansoni</i> naturally results from site- and tissue- specific immunological and biochemical responses to the egg-derived antigens and molecules and suggested that the intestines appear to harbor immune-privileged sites.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0036224"},"PeriodicalIF":2.9,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629614/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142667757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Article of Significant Interest in This Issue.","authors":"","doi":"10.1128/iai.00552-24","DOIUrl":"10.1128/iai.00552-24","url":null,"abstract":"","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":"92 12","pages":"e0055224"},"PeriodicalIF":2.9,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11640281/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}