The functional role of spleen neutrophil-like cells in the immune response to allogeneic tumor cells

2007 ◽  
Vol 414 (1) ◽  
pp. 242-245 ◽  
Author(s):  
E. V. Maryukhnich ◽  
E. S. Zvezdova ◽  
T. V. Anfalova ◽  
L. M. Khromykh ◽  
D. B. Kazansky
Keyword(s):  
Immune Response ◽  
Tumor Cells ◽  
Functional Role ◽  
Allogeneic Tumor

scholarly journals NLRP7 Promotes Choriocarcinoma Growth and Progression through the Establishment of an Immunosuppressive Microenvironment

Cancers ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2999
Author(s):  
Deborah Reynaud ◽  
Roland Abi Nahed ◽  
Nicolas Lemaitre ◽  
Pierre-Adrien Bolze ◽  
Wael Traboulsi ◽  
...  
Keyword(s):  
Immune Response ◽  
Tumor Cells ◽  
Major Gene ◽  
Critical Role ◽  
Orthotopic Model ◽  
Independent Manner ◽  
Maternal Immune Response ◽  
The Impact

The inflammatory gene NLRP7 is the major gene responsible for recurrent complete hydatidiform moles (CHM), an abnormal pregnancy that can develop into gestational choriocarcinoma (CC). However, the role of NLRP7 in the development and immune tolerance of CC has not been investigated. Three approaches were employed to define the role of NLRP7 in CC development: (i) a clinical study that analyzed human placenta and sera collected from women with normal pregnancies, CHM or CC; (ii) an in vitro study that investigated the impact of NLRP7 knockdown on tumor growth and organization; and (iii) an in vivo study that used two CC mouse models, including an orthotopic model. NLRP7 and circulating inflammatory cytokines were upregulated in tumor cells and in CHM and CC. In tumor cells, NLRP7 functions in an inflammasome-independent manner and promoted their proliferation and 3D organization. Gravid mice placentas injected with CC cells invalidated for NLRP7, exhibited higher maternal immune response, developed smaller tumors, and displayed less metastases. Our data characterized the critical role of NLRP7 in CC and provided evidence of its contribution to the development of an immunosuppressive maternal microenvironment that not only downregulates the maternal immune response but also fosters the growth and progression of CC.

Intestinal dysbiosis augments liver disease progression via NLRP3 in a murine model of primary sclerosing cholangitis

Gut ◽  
2019 ◽  
Vol 68 (8) ◽  
pp. 1477-1492 ◽  
Author(s):  
Lijun Liao ◽  
Kai Markus Schneider ◽  
Eric J C Galvez ◽  
Mick Frissen ◽  
Hanns-Ulrich Marschall ◽  
...  
Keyword(s):  
Immune Response ◽  
Liver Injury ◽  
Sclerosing Cholangitis ◽  
Functional Role ◽  
Innate Immune ◽  
Caspase 8 ◽  
Inflammasome Activation ◽  
Intestinal Dysbiosis ◽  
Nlrp3 Inflammasome Activation

ObjectiveThere is a striking association between human cholestatic liver disease (CLD) and inflammatory bowel disease. However, the functional implications for intestinal microbiota and inflammasome-mediated innate immune response in CLD remain elusive. Here we investigated the functional role of gut–liver crosstalk for CLD in the murine Mdr2 knockout (Mdr2−/−) model resembling human primary sclerosing cholangitis (PSC).DesignMale Mdr2−/−, Mdr2−/− crossed with hepatocyte-specific deletion of caspase-8 (Mdr2−/−/Casp8∆hepa) and wild-type (WT) control mice were housed for 8 or 52 weeks, respectively, to characterise the impact of Mdr2 deletion on liver and gut including bile acid and microbiota profiling. To block caspase activation, a pan-caspase inhibitor (IDN-7314) was administered. Finally, the functional role of Mdr2−/−-associated intestinal dysbiosis was studied by microbiota transfer experiments.ResultsMdr2−/− mice displayed an unfavourable intestinal microbiota signature and pronounced NLRP3 inflammasome activation within the gut–liver axis. Intestinal dysbiosis in Mdr2−/− mice prompted intestinal barrier dysfunction and increased bacterial translocation amplifying the hepatic NLRP3-mediated innate immune response. Transfer of Mdr2−/− microbiota into healthy WT control mice induced significant liver injury in recipient mice, highlighting the causal role of intestinal dysbiosis for disease progression. Strikingly, IDN-7314 dampened inflammasome activation, ameliorated liver injury, reversed serum bile acid profile and cholestasis-associated microbiota signature.ConclusionsMDR2-associated cholestasis triggers intestinal dysbiosis. In turn, translocation of endotoxin into the portal vein and subsequent NLRP3 inflammasome activation contribute to higher liver injury. This process does not essentially depend on caspase-8 in hepatocytes, but can be blocked by IDN-7314.

THE IMMUNE RESPONSE OF MICE REPEATEDLY INJECTED WITH ALLOGENEIC TUMOR CELLS

1975 ◽  
Vol 20 (5) ◽  
pp. 399-403 ◽  
Author(s):  
S. T. SONIS ◽  
P. STELOS ◽  
S. E. BEAR ◽  
M. A. FITZGERALD ◽  
R. E. WILSON
Keyword(s):  
Immune Response ◽  
Tumor Cells ◽  
Allogeneic Tumor

scholarly journals Role of alloantigens in natural killing. Allogeneic but not autologous tumor biopsy cells are sensitive for interferon-induced cytotoxicity of human blood lymphcoytes.

1980 ◽  
Vol 151 (5) ◽  
pp. 1151-1165 ◽  
Author(s):  
F T Vánky ◽  
S A Argov ◽  
S A Einhorn ◽  
E Klein
Keyword(s):  
Tumor Cells ◽  
Antigen Expression ◽  
Autologous Tumor ◽  
Tumor Biopsy ◽  
Allogeneic Tumor ◽  
Healthy Donors ◽  
Immunological Recognition ◽  
Quantitative Changes ◽  
Killing Function

Blood lymphocytes of patients with solid tumors were assayed for cytotoxicity against autologous and allogeneic primary tumor cells. The lymphocytes killed autologous tumor cells in 7 of 25 cases (28%) and allogeneic tumor cells in 2 of 37 tests (5%). Lymphocytes from healthy donors were rarely cytotoxic for the biopsy cells, which indicates that these cells have low natural kill sensitivity. The autoreactivity that may reflect the immunological recognition of tumor cells was not altered by pretreatment of the effectors with interferon (IF). In contrast, killing of allogeneic tumor biopsy cells was induced by IF in approximately 50% of tests, with the lymphocytes of both the tumor patients and the healthy donors. The mechanism of the alloreactivity is most likely a consequence of IF-induced polyclonal activation of cytotoxic potential and the lymphocytes that are committed to recognize the alloantigens expressed on the particular target manifest the killing function. When the biopsy cells were explanted and kept in culture for 5-6 d, their susceptibility for the lymphocyte damage increased, and they were killed by the IF-treated cells also in autologous combinations. Whether this change in sensitivity is a result of qualitative or quantitative changes in antigen expression or of other changes in the properties of the cell membrane is unknown.

Functional role of the Ca2+-activated Cl− channel DOG1/TMEM16A in gastrointestinal stromal tumor cells

2014 ◽  
Vol 326 (2) ◽  
pp. 315-325 ◽  
Author(s):  
Erik Berglund ◽  
Pinar Akcakaya ◽  
David Berglund ◽  
Fredrik Karlsson ◽  
Vladana Vukojević ◽  
...  
Keyword(s):  
Gastrointestinal Stromal Tumor ◽  
Tumor Cells ◽  
Functional Role ◽  
Stromal Tumor ◽  
Cl Channel

scholarly journals Identification of Regulatory Functions of LncRNAs Associated With T. circumcincta Infection in Adult Sheep

2021 ◽  
Vol 12 ◽  
Author(s):  
Praveen Krishna Chitneedi ◽  
Rosemarie Weikard ◽  
Juan J. Arranz ◽  
María Martínez-Valladares ◽  
Christa Kuehn ◽  
...  
Keyword(s):  
Immune Response ◽  
Functional Role ◽  
Defense Mechanism ◽  
Nematode Infection ◽  
Cellular Growth ◽  
Differentially Expressed ◽  
Differential Host ◽  
Adult Sheep ◽  
Gene Enrichment

Several recent studies have demonstrated the role of long non-coding RNAs (lncRNAs) in regulating the defense mechanism against parasite infections, but no studies are available that investigated their relevance for immune response to nematode infection in sheep. Thus, the aim of the current study was to (i) detect putative lncRNAs that are expressed in the abomasal lymph node of adult sheep after an experimental infection with the gastrointestinal nematode (GIN) Teladorsagia circumcincta and (ii) to elucidate their potential functional role associated with the differential host immune response. We hypothesized that putative lncRNAs differentially expressed (DE) between samples from animals that differ in resistance to infection may play a significant regulatory role in response to nematode infection in adult sheep. To obtain further support for our hypothesis, we performed co-expression and functional gene enrichment analyses with the differentially expressed lncRNAs (DE lncRNAs). In a conservative approach, we included for this predictive analysis only those lncRNAs that are confirmed and supported by documentation of expression in gastrointestinal tissues in the current sheep gene atlas. We identified 9,105 putative lncRNA transcripts corresponding to 7,124 gene loci. Of these, 457 were differentially expressed lncRNA loci (DELs) with 683 lncRNA transcripts. Based on a gene co-expression analysis via weighted gene co-expression network analysis, 12 gene network modules (GNMs) were found significantly correlated with at least one of 10 selected target DE lncRNAs. Based on the principle of “guilt-by-association,” the DE genes from each of the three most significantly correlated GNMs were subjected to a gene enrichment analysis. The significant pathways associated with DE lncRNAs included ERK5 Signaling, SAPK/JNK Signaling, RhoGDI Signaling, EIF2 Signaling, Regulation of eIF4 and p70S6K Signaling and Oxidative Phosphorylation pathways. They belong to signaling pathway categories like Cellular Growth, Proliferation and Development, Cellular Stress and Injury, Intracellular and Second Messenger Signaling and Apoptosis. Overall, this lncRNA study conducted in adult sheep after GIN infection provided first insights into the potential functional role of lncRNAs in the differential host response to nematode infection.

The role of bacterial super antigens in the immune response: From biology to cancer treatment

2020 ◽  
Vol 16 ◽  
Author(s):  
Behnam Emamgolizadeh Gurt Tapeh ◽  
Mohammad Sadegh Hashemzadeh ◽  
Ali Mir Hoseini
Keyword(s):  
Immune Response ◽  
Immune System ◽  
T Lymphocytes ◽  
Cancer Treatment ◽  
Tumor Cells ◽  
Vector Systems ◽  
Bacterial Vector ◽  
Antigen Presenting ◽  
Stimulation Of

Aims: Encouraging results have been indicated preclinically and in patients using the bacterial super antigen. This review article intends to summarize the role of the super antigens that have been recently used in the treatment of cancer. In addition, the vector systems including lentiviral vectors, adeno-associated vector systems and retroviral vectors that are increasingly being used in basic and applied research were discussed. Most importantly, the new CRISPR technique has also been discussed in this literature review. Discussion: More successful therapies can be achieved by manipulating bacterial vector systems through incorporating genes related to the super antigens and cytokines. The products of SAg and cytokine genes contributes to the strong stimulation of immune system against tumor cells. They bind to MHC II molecules as well as the V beta regions of TCR and lead to the production of IL2 and other cytokines, the activation of antigen-presenting cells and T lymphocytes. Additionally, super antigens can be used to eradicate tumor cells. Better results in cancer treatment can be achieved by transferring super antigen genes and subsequent strong immune stimulation along with other cancer immunotherapy agents. Conclusion: Super antigens induce the proliferation of T lymphocytes and antigen-presenting cells by binding to MHCII molecules and V beta regions in T cell receptors. Therefore, the presentation of tumor cell antigens is increased. Additionally, the production of important cytokines by T cells and APCs contributes to the stimulation of immune response against tumor cells. The manipulation of bacterial vector systems through incorporating genes related to SAgs and other immune response factors is a good strategy for immune system stimulating and eradicating of tumor cells along with other immunotherapy agents.

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