Journal of cellular immunology最新文献

{"title":"B cells are Essential for Memory T cell Development in Germinal Centers.","authors":"Gongyi Zhang","doi":"10.33696/immunology.8.257","DOIUrl":"https://doi.org/10.33696/immunology.8.257","url":null,"abstract":"<p><p>Nature recently listed 20 major T cell milestones since the early breakthroughs of Drs. Jacques Miller and Max Cooper. However, to make the story more complete, several key discoveries may need to be mentioned. One of the major missing episodes is the discovery of the bone marrow in mice as the origin of T and B cells, revealed by Dr. Henry Claman and his colleagues. The complete absence of the critical role of B cells in the final differentiation of T cells into memory lineages could be a major oversight in modern immunology. In this short essay, I will try to summarize some of the published evidence showing that T cell differentiation into memory cells is triggered only by B cells in germinal centers after priming at infection sites for CD8 T cells and in the T cell zone for CD4 T cells in the spleen and draining lymph nodes. Based on the analysis, T cells need two steps to develop into long-lived memory cells, and a new T cell lineage model is presented.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"8 2","pages":"81-86"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13662902/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149198196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Commentary on Dual Orphan Nuclear Receptor 4A1 (NR4A1) and NR4A2 Ligands.","authors":"Stephen Safe, James J Cai, Robert S Chapkin","doi":"10.33696/immunology.8.251","DOIUrl":"10.33696/immunology.8.251","url":null,"abstract":"<p><p>1,1-Bis(3'-indolyl)-1-(3,5-disubstitutedphenyl)methane (DIM-3,5) compounds in the presence or absence of a 4-hydroxylphenyl group bind both orphan nuclear receptor 4A1 (NR4A1) and NR4A2. In cancer cells, these compounds bind and inactivate pro-oncogenic NR4A1 and NR4A2 and downstream pathways acting as inverse agonists that inhibit cancer cell growth, survival, migration and invasion, and induce ferroptosis. Similar results are observed in endometriotic cells where the DIM-3,5 dual NR4A1/2 ligands inhibit NR4A1/NR4A2-mediated pro-endometriotic genes and pathways. The potency of these DIM-3,5 dual NR4A1/NR4A2 ligands is also observed in tumor infiltrating lymphocytes where both receptors are expressed and regulate comparable functions.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"8 1","pages":"30-36"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13293520/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148334990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding the Mechanistic Connection between Dysbiosis and Polyamine Regulation in Oral and Intestinal Inflammation- Role of Tregs and Th17 Cells.","authors":"Pushpa Pandiyan","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Periodontitis and inflammatory bowel disease (IBD) are chronic inflammatory conditions driven by dysbiotic microbial communities that subvert host mucosal immunity. Central to the immunopathology of both diseases is the disruption of the balance between regulatory T cells (Tregs) and T helper 17 (Th17) cells, an equilibrium that governs tissue homeostasis versus inflammatory destruction. Polyamines, principally putrescine (PUT), spermidine (SPD), and spermine (SPN), are emerging as critical immunometabolic regulators that modulate the plasticity and functional identity of both cell populations. Dysbiosis, particularly the enrichment of microbial communities that drive aberrant polyamine biosynthesis through ornithine decarboxylase (ODC)-dependent pathways, generates a polyamine-rich microenvironment that further dysregulates T cell function and promotes sustained inflammation. Experimental evidence demonstrates that mucosal polyamine levels correlate with dysbiosis, dysfunctional Treg (TregDys) expansion, and CD4⁺CD4⁺T cell hyperactivation, collectively contributing to and perpetuating chronic inflammation. The striking parallels between periodontitis and IBD reinforce the existence of conserved mechanisms linking mucosal dysbiosis to polyamine-driven immune dysregulation, with shared therapeutic implications for targeting the dysbiosis-T cell-polyamine axis to restore immune homeostasis. This review presents a unified mechanistic framework connecting oral and intestinal dysbiosis, polyamine dysregulation, and disruption of the Treg/Th17 balance, linking both diseases along the oral-gut axis.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"8 2","pages":"65-73"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13614437/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149066475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Ability of Neonatal Mice to Develop Immunity to <i>Mycobacterium tuberculosis</i> Shows Sex Differences, with Females Displaying Evidence of an Enhanced Immune Response.","authors":"Mrinal K Ghosh, Ameae M Walker","doi":"10.33696/immunology.7.225","DOIUrl":"10.33696/immunology.7.225","url":null,"abstract":"<p><p>Using four core genotypes (FCG) mice, we have previously shown a larger number of CD4⁺ and CD8⁺ T cells in the spleens of female mice, a sex difference that develops by postnatal day 7 and is retained through adulthood. This difference in splenic T cell number is a consequence of reduced thymic egress and reduced splenic seeding in male mice, caused in part by the male-specific perinatal surge of testosterone, and in part by <i>Sry</i>, which is overexpressed in this model. Here, we used the background strain for FCG mice (C57BL/6J) to ask whether sex influenced actual immunity in the postnatal period. Pups were immunized on postpartum days 1 or 3 with <i>Mycobacterium tuberculosis</i> (Mtb), challenged on day 7 with Mtb purified protein derivative (PPD), and sacrificed on day 8. Subsequent <i>ex vivo</i> challenges of splenocytes showed PPD-stimulated CD8⁺ responses (increased CD8⁺, increased CD8⁺CD44^hi, decreased CD8⁺CD44^hiCD127^-/lo) but no differences between males and females. However, when CD8⁺ T cells were analyzed for IFN-γ and IL-2 production, although there was no sex difference in mono-functional IFN-γ⁺ (100%) or IL-2⁺ (67%), only females (0% of males and 42% of females) produced bi-functional (IFN-γ⁺IL-2⁺) cells. <i>Ex vivo</i> PPD-stimulated responses of other relevant cells from the spleen showed no sex differences in dendritic cells (CD11c⁺CD86⁺IL-6⁺) but females had more (3-fold) IL-6-producing macrophages (F4/80⁺CD86⁺IL-6⁺) and reduced T regulatory cells (CD4⁺CD25⁺Foxp3⁺). We conclude that some sex differences in immunity are evident at one week of age in Mtb immunized mouse pups, with females exhibiting qualitatively superior Mtb-specific immune responses.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"7 2","pages":"52-63"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12356363/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144877151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammatory, Functional, and Compositional Changes of the Uterine Immune Microenvironment in a Lymphangioleiomyomatosis Mouse Model.","authors":"Danielle S Stiene, Andrew R Osterburg, Lori B Corsarie, Nick R Balzarini, Mario Medvedovic, Michael T Borchers","doi":"10.33696/immunology.7.227","DOIUrl":"10.33696/immunology.7.227","url":null,"abstract":"<p><p>Lymphangioleiomyomatosis (LAM) is a rare, female-dominated pulmonary cystic disease. Cysts that develop in LAM are characterized by the presence of smooth muscle-like (LAMCore) cells in the periphery. These cells harbor mutations in <i>Tuberous Sclerosis Complex 1</i> or <i>2</i> (<i>TSC1/2</i>), driving uncontrolled proliferation through the mTORC1 pathway. LAMCore cells originate from an extrapulmonary source. Published data supports the uterine origin of LAMCore cells that metastasize from the uterus to precipitate pulmonary function destruction. Immune evasion is hypothesized to occur to allow seeding of the lungs from the uterus. This evasion specifically involves dysfunctional NK cells to allow aberrant proliferation and migration from the tissue. Single-cell RNA sequencing revealed changes in chemokine and cytokine protein and receptor expression in uterine NK (uNK) and other immune cell populations in a uterine-specific <i>Tsc2</i>-knockout mouse model of LAM. ELISA data revealed increased concentrations of multiple pro-inflammatory cytokines in the sera of aged <i>Tsc2</i>-knockout mice. Flow cytometry, IHC, and functional assays identified compositional and functional insufficiencies of the uNK cells in <i>Tsc2</i>-knockout mice. Furthermore, depletion of NK cells led to the increased development of pulmonary metastases. These data suggest an inflammatory feedback loop affecting multiple cell types including uNK cells, macrophages, and neutrophils. This leads to alterations in immune cell function and composition which allow for LAMCore cell metastasis from the uterine tissue, which may provide a novel mechanism for LAM development.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"7 3","pages":"74-97"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12392152/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Urinary <i>Borrelia</i> peptides correlate with the General Symptom Questionnaire (GSQ-30) scores in symptomatic patients with suspicion of tick-borne illness.","authors":"Sindhu Datla, Sumaiya Irfan, Nicole Trumbull, Rocio Cornero, Ahana Byne, Ghaliah Alluhaibi, Claudius Mueller, Ruben Magni, Weidong Zhou, Barbara Birkaya, Lance Liotta, Alessandra Luchini, Hope McIntyre","doi":"10.33696/immunology.7.218","DOIUrl":"10.33696/immunology.7.218","url":null,"abstract":"<p><strong>Background: </strong><i>Borreliosis</i> infection and post-treatment Lyme disease syndrome are associated with nonspecific, multisystem symptoms, and there is currently no effective direct test for Lyme disease. The seroprevalence of <i>Borrelia miyamotoi</i> among individuals with suspected tick-borne illnesses and persistent symptoms is not well documented. Although bacterial extracellular vesicles (BEVs) have been suggested as potential sources of disease biomarkers, evidence supporting their role in <i>Borrelia</i> infection is lacking.</p><p><strong>Methods: </strong>Patients (N=66) with symptoms and with clinical suspicion of a tick-borne illness were enrolled in the study and followed longitudinally over the course of 1 year (min 1 visit, max 4 visits). The General Symptom Questionnaire (GSQ-30) was administered to the patients at each visit to measure symptom burden. Lyme and <i>Borrelia miyamotoi</i> serologies were conducted at LabCorp or Quest, under the standard of care. A mass spectrometry proteomic assay measuring <i>Borrelia</i>-specific peptides was conducted in the urine of the patients.</p><p><strong>Results: </strong>Among the analyzed patients, 65% had positive Lyme serology and 33% had positive <i>B. miyamotoi</i> serology with partial overlap (20%). Urinary <i>Borrelia</i>-specific peptides correlated with the GSQ-30 score after correcting for age, Lyme serology, and <i>B. miyamotoi</i> serology (coefficient = 0.57, t-test p-value < 0.00001). Urinary extracellular vesicles had positive reactivity in a p66 immunoassay, a known marker of <b><i>Borrelia</i></b> BEVs. Urinary peptides included glycerophosphodiester phosphodiesterase, variable small and large outer membrane proteins, the multicopy lipoprotein family, and <i>Borrelia</i> direct repeat proteins, which are also known markers of <i>Borrelia</i> BEVs.</p><p><strong>Conclusions: </strong>The <i>B. miyamotoi</i> seroprevalence (33%) in a symptomatic population with clinical suspicion of a tick-borne illness was higher than the seroprevalence estimated from previous studies. As it provides an objective measurement correlated with a standardized symptom burden score, urinary <i>Borrelia</i> peptide detection offers a promising avenue for future assay development. This proteomic analysis supported the presence of <i>Borrelia</i> BEVs in the urine of symptomatic patients with suspected tick-borne illnesses.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"7 1","pages":"14-25"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13449241/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148698289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum Cytokines During Acute Respiratory Infection and Relationship to Age.","authors":"Aanya Gupta, Holden T Maecker","doi":"10.33696/immunology.7.234","DOIUrl":"10.33696/immunology.7.234","url":null,"abstract":"<p><p>Influenza and other seasonal respiratory viruses affect millions annually. While age is generally known to be correlated with risk and outcome, the mechanisms underlying these differences, especially in the infected, have been poorly defined. Previous studies have focused primarily on cell-subset shifts in older adults, leaving a gap in understanding of how cytokine responses vary across the full age spectrum. Cytokine data from Luminex assays were compiled from Stanford clinical studies and after batch control filtering, the dataset included 181 healthy individuals (ages 4-97) and 27 symptomatic individuals (mostly confirmed influenza, ages 14-77). Ordinary least squares regression was applied to assess cytokine differences due to infection status, age, and their interaction, with statistical significance defined as p<0.05. The results illustrated that pro-inflammatory cytokines were found to be significantly elevated in infected individuals, with a trend of stronger effects in the young supported by comparison of intercepts between the regressions for the healthy and infected cohorts. The concept of inflammaging was also seen through several biomarkers with significant non-zero slopes in healthy cohorts that were not well-established in prior research. Our findings reveal both expected and novel cytokine behavior in influenza infection across a wide range of ages. By incorporating younger individuals and including age as a continuous variable, the study makes progress towards a deeper understanding of the changes in the immune system and its response to influenza across the lifespan.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"7 4","pages":"139-145"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12811030/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145999832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Salivary Lymphocyte Phenotypes Differ from Blood and Serve as a Model for Other Mucosal Fluids.","authors":"Muruganantham Lillimary Eniya, Shervin Dokht Sadeghi Nasab, Albert Judith, Frederick Clasen, David Moyes, Saeed Shoaie, Newell Johnson, Priya Kannian, Stephen Challacombe","doi":"10.33696/immunology.7.233","DOIUrl":"10.33696/immunology.7.233","url":null,"abstract":"<p><strong>Background & objectives: </strong>The oral cavity is part of the mucosal immune system of the body, embracing all mucosae including lungs, gut and nose. The oral mucosa is the gateway for a plethora of gastrointestinal and respiratory antigens and is capable of mounting a very strong mucosal immune response. Mucosal immunity is structurally and functionally similar in all mucosae and, soluble mediators including cytokines, chemokines, immunoglobulins and other proteins have been well studied in many diseases. However, the roles of mucosal immune cell phenotypes remain less studied causing setbacks in our understanding of the disease pathogeneses.</p><p><strong>Methods: </strong>We have reviewed the importance of immune phenotyping of the cells in mucosal secretions and the employment of flow cytometry as a reliable tool for this purpose. We previously showed that CD3, CD4, CD8, Th1, and Th2 cells can be detected in stimulated whole mouth fluid (SWMF) in a reproducible and consistent manner, and their ratios may differ from those in the peripheral circulation. We now show for the first time that other salivary lymphocytes Th17, Th22, Tfh, Tregs, NKT, NK, ILC1, ILC2, and ILC3 cells can also be detected and quantified using flow cytometry. PBMC and SWMF from 119 participants were tested by flow cytometry.</p><p><strong>Results: </strong>Mean frequencies of all the immune cells were detected in a reproducible and consistent manner. In the SWMF the mean frequencies of Th17, Th22, Tfh and NK cells were greater than PBMC. These phenotypes in SWMF showed a negative correlation with PBMC suggesting mucosal origin and specificity.</p><p><strong>Conclusions: </strong>Our findings strongly suggest that flow cytometry can be employed to detect a wide range of lymphocyte phenotypes in SWMF, a hypotonic secretion. Due to the similarities among the various mucosal secretions, this technique could be explored as a promising tool for understanding immunopathogenesis of infectious and non-infectious diseases using mucosal secretions.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"7 4","pages":"133-138"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7618796/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147313351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From Bench to Body: Protective <i>Candida</i>-specific Monoclonal Antibodies Show <i>In vivo</i> and Translational Potential.","authors":"Hong Xin","doi":"10.33696/immunology.7.231","DOIUrl":"10.33696/immunology.7.231","url":null,"abstract":"<p><p><i>Candida auris</i> is a multidrug-resistant fungal pathogen that presents a growing global health challenge, particularly due to its ability to cause invasive bloodstream and deep-seated infections in vulnerable patients. Monoclonal antibody (mAb)-based immunotherapy offers a novel and targeted approach to overcoming the limitations of current antifungal treatments. This commentary highlights the protective efficacy of <i>Candida</i>-specific mAbs, C3.1, 6H1, and 9F2, in <i>in vivo</i> mouse models of disseminated candidiasis. These antibodies target distinct, conserved surface antigens and significantly reduce fungal burden while improving survival outcomes. Their translational potential lies in their specificity, low toxicity, and ability to enhance host immune responses, making them strong candidates for future development as adjunct or alternative therapies for invasive fungal infections in humans.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"7 3","pages":"122-126"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12463460/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145187717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"VEGF-D Dependent IFNγ Production by Natural Killer Cells in Lymphangioleiomyomatosis.","authors":"Andrew R Osterburg, Morgan A Terry, Danielle S Stiene, Racheal Foot, Rebecca L Nelson, Michael T Borchers","doi":"10.33696/immunology.7.242","DOIUrl":"10.33696/immunology.7.242","url":null,"abstract":"<p><p>Lymphangioleiomyomatosis (LAM) is a rare cystic neoplasm that almost exclusively affects women. LAM arises from inherited or spontaneous mutations in <i>TSC1</i> or <i>TSC2</i> genes, which result in constitutive activation of mTOR and downstream signaling. These mutations arise in a uterine population of cells that migrate to the lungs where they establish nodules that progress to cysts and progressive lung function decline. Clinically, an elevated level (>800 pg/ml) of vascular endothelial growth factor -D (VEGF-D) is a definitive diagnostic marker for LAM. Recent work by our group and others highlights the role of immune dysfunction in the establishment and progression of LAM. A subset of natural killer (NK) cells in LAM express the VEGF-D receptors, VEGFR3 and NRP2. These distinct NK cells are responsive to VEGF-D treatment and LAM NK cells have altered NKG2D and CD160 expression, as well as changes in phosphorylation of STAT4(Y693) and ERK1/2 (Y202/S204). Phosphorylation of these proteins increases after VEGF-D treatment at short time points (0-30 min) and longer time points (up to 6 hours). In addition, the signaling kinetics are altered compared to cytokine stimulation. Increased IFNγ production was shown by ELISA and flow cytometry after VEGF-D, and other cytokines. Baseline IFNγ expression is higher in LAM NK cells, and LAM NK cells elaborate IFNγ when stimulated with VEGF-D. Additionally, these NK cells have increased responsiveness to IL12/33 and decreased responsiveness to IL12/IL27 co-stimulation. These data demonstrate that NK cells from LAM patients are functionally altered and these changes in baseline function may contribute to disease progression and pathology.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"7 6","pages":"204-215"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13166106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147935612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}