B lymphocytes (B cells) play a complex and paradoxical role in tumorigenesis. They can recognize tumor-associated antigens, present these antigens to T cells, and produce antibodies that directly target and eliminate tumor cells. This makes B cells a potentially powerful ally in combating cancer. However, B cells also exhibit immunosuppressive functions, secreting cytokines like IL-10 or generating tumor-promoting antibodies that dampen the anti-tumor immune response, and some tumor cells have even been shown to exploit B cells to promote their growth and metastasis. This dual nature of B cells presents both opportunities and challenges for tumor immunotherapy. In this review, we summarize the mechanisms underlying the multifaceted functions of B cells and their current applications in cancer immunotherapy. Furthermore, we also explore the key issues and future directions in this field, emphasizing the need for further research to fully harness the anti-tumor potential of B cells in the fight against cancer.
Humans ; B-Lymphocytes/immunology* ; Neoplasms/therapy* ; Carcinogenesis/immunology* ; Immunotherapy/methods* ; Animals

Granulocyte colony-stimulating factor (G-CSF) is an essential regulator of neutrophil trafficking and is highly expressed in multiple tumors. Myeloid derived suppressor cells (MDSCs) promote neoplastic progression through multiple mechanisms by immune suppression. Despite the findings of G-CSF function in colon cancer progression, the precise mechanism of G-CSF on MDSCs regulation and its blockade effects on tumor growth remains a worthy area of investigation. In this study we observed an overexpression of G-CSF in a mouse colitis-associated cancer (CAC) model, which was consistent with the accumulation of MDSCs in mouse colon tissues. Further in vitro studies demonstrated that G-CSF could promote MDSCs survival and activation through signal transducer and activator of transcription 3 (STAT3) signaling pathway. Moreover, compared with isotype control, anti-G-CSF mAb treatment demonstrated reduced MDSC accumulation, which led to a marked decrease in neoplasm size and number in mice. Our results indicated that G-CSF is a critical regulating molecule in the migration, proliferation and function maintenance of MDSCs, which could be a potential therapeutic target for colitis-associated cancer.
Animals ; Carcinogenesis ; Colitis ; complications ; Colorectal Neoplasms ; complications ; drug therapy ; immunology ; metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Granulocyte Colony-Stimulating Factor ; genetics ; metabolism ; Immunotherapy ; Mice ; Molecular Targeted Therapy ; Myeloid Cells ; immunology ; metabolism ; pathology

Prevention of infection by the human papillomavirus (HPV) has become a hot research topic since the relationship between the HPV and cervical cancer was confirmed. Persistent infection with HPV and early expression of proteins has an important role in the pathogenesis of cervical cancer. Vaccines that protect against four high-risk types of HPV (-6, -11, -16, -18) have been used worldwide. A bivalent vaccine (HPV-16 and -18) developed by Walvax is in clinical trials. This study reviews progress in ascertainment of the structure and function of the HPV genome, the molecular mechanism of carcinogenesis, and vaccines based on virus-like particles.
Animals ; Carcinogenesis ; Female ; Humans ; Papillomaviridae ; genetics ; immunology ; metabolism ; Papillomavirus Infections ; pathology ; prevention & control ; virology ; Papillomavirus Vaccines ; genetics ; immunology ; Uterine Cervical Neoplasms ; pathology ; prevention & control ; virology ; Viral Proteins ; genetics ; immunology ; metabolism

Ulcerative colitis is a non-specific colorectal inflammation of unknown causes. It is now known to complicate the dangers of colorectal cancer more than was previously thought. Macrophages are an important part of immune system and play a positive role in immune reaction. But it has been shown that the phenotype and the function of macrophages change in the tumor microenvironment. Through their interaction with colorectal cancer cells and by releasing large quantities of cytokines, macrophages promote colorectal cancer cells by inhibiting angiogenesis and inhibit apoptosis. But the macrophages are also affected by cancer, interact with other inflammatory cells, and become immune suppressed. Thus the changes of macrophages are inseparable with colitis-associated colorectal carcinogenesis.
Carcinogenesis ; Cell Transformation, Neoplastic ; immunology ; Colitis, Ulcerative ; complications ; immunology ; pathology ; Colorectal Neoplasms ; etiology ; immunology ; pathology ; Disease Progression ; Humans ; Macrophages ; pathology

PURPOSE : Cyclooxygenase-2 (COX-2) and its metabolite, PGE2 affect multiple tumorigenesis, including angiogenesis, invasion, and tumor-induced immune suppression. Their overexpression is association with impaired immune cell function in many tumors. Indoleamine 2,3-dioxygenase (IDO) is an emerging immuno-regulatory enzyme that can catalyze the initial rate-limiting step in tryptophan catabolism, by causing tryptophan depletion can block T lymphocyte activation, and thus, enable tumor cells to escape from immune system. Although the potential of immunosuppression associated with tumorproduced COX-2 has been suggested, the mechanism of immunosuppression in tumor immunology is not yet well defined. Thus, we hypothesized that the tumor immunity of COX-2 could be partly due to IDO-dependent immune tolerance. To test this hypothesis, we evaluated IDO expression in cancer cells treated with selective COX-2 inhibitor. MATERIALS AND METHODS : The A549 human adenocarcinoma cell line, murine Lewis lung carcinoma (LLC) cell line and C57Bl/6 mice were used for in vitro and in vivo studies. In vitro studies, A549 cells were treated with various concentrations of COX-2 inhibitor (PTPBS) or PGE2. IDO enzyme activity and protein expression were checked by IDO enzyme activity assay and Western blotting. In vivo study, the 20 mice were randomized into normal control, LLC inoculated control, and low and high selective COX-2 inhibitor (celecoxib 25 or 250 mg/kg/day) treated LLL inoculated mice groups (n=5 per group). At one month, mice were sacrificed and tumor mass was isolated for quantification of IDO expression by immunohistochemical stain and western blotting. RESULTS : In vitro studies, PTPBS treated A549 cells showed a significant decreased in IDO enzyme activity and expression but PGE2 treated A549 cells showed increased in IDO expression. In vivo studies, the tumor mass and lung metastasis were attenuated by celecoxib (respectively, p<0.05, p<0.01). Compared with the LLC inoculated control group, mice treated with celecoxib had significant reductions in IDO expression of tumor mass (IDO immunohistochemical stain and western blotting ). CONCLUSION : The present study reveals that COX-2 inhibitor serves to restore the tumor-induced IDO expression and promotes antitumor reactivity in an immunocompetent murine lung cancer model. These findings further support the suggestion that COX-2 inhibitor is a potential pharmacological immunotherapy in cancer
Adenocarcinoma ; Allergy and Immunology ; Animals ; Blotting, Western ; Carcinogenesis ; Carcinoma, Lewis Lung ; Cell Line ; Cyclooxygenase 2* ; Dinoprostone ; Humans ; Immune System ; Immune Tolerance* ; Immunosuppression ; Immunotherapy ; Indoleamine-Pyrrole 2,3,-Dioxygenase* ; Lung ; Lung Neoplasms ; Lymphocyte Activation ; Metabolism ; Mice ; Neoplasm Metastasis ; Tryptophan ; United Nations ; Celecoxib