Leukocyte composition of pronephros of Leocottus kesslerii infected with hemoflagellates of the genus Trypanosoma (Kinetoplastea: Trypanosomatida)

This study determined for the first time the changes in leukocyte composition of the pronephros (head kidney) of sand sculpin Leocottus kesslerii, (Sideleva, 2001) (Lake Gusinoye, Lake Baikal basin, Eastern Siberia, Russia), infected and uninfected with hemoflaggellates of the genus Trypanosoma. The results indicated that the trypanosomes modulated the development of the immune response of their host (suppression of B cell immunity and granulocytic reactions, activation of the leucopoiesis and monocytopoiesis). Selective suppression of immune response in host with trypanosomes promotes the survival and development of parasites.

An immunotherapeutic approach to decipher the role of long non-coding RNAs in cancer progression, resistance and epigenetic regulation of immune cells

Immunotherapeutic treatments are gaining attention due to their effective anti-tumor response. Particularly, the revolution of immune checkpoint inhibitors (ICIs) produces promising outcomes for various cancer types. However, the usage of immunotherapy is limited due to its low response rate, suggesting that tumor cells escape the immune surveillance. Rapid advances in transcriptomic profiling have led to recognize immune-related long non-coding RNAs (LncRNAs), as regulators of immune cell-specific gene expression that mediates immune stimulatory as well as suppression of immune response, indicating LncRNAs as targets to improve the efficacy of immunotherapy against tumours. Moreover, the immune-related LncRNAs acting as epigenetic modifiers are also under deep investigation. Thus, herein, is a summarised knowledge of LncRNAs and their regulation in the adaptive and innate immune system, considering their importance in autophagy and predicting putative immunotherapeutic responses.

Tumor-macrophage crosstalk: how to listen

The tumor microenvironment contains many cellular components influencing tumor behaviors, such as metastasis, angiogenesis and chemo-resistance. Tumor-associated macrophages (TAMs) are one of such components that can also manipulate the overall prognosis and patient survival. Analysis of tumor-macrophage crosstalk is crucial as tumor cells can polarize circulatory monocytes into TAMs. Such trans-polarization of macrophages support tumor mediated evasion and suppression of immune response. Additionally, such TAMs significantly influence tumor growth and proliferation, making them a potential candidate for precision therapeutics. However, the failure of macrophage-dependent therapies at clinical trials emphasizes the fault in current perception and research modality. This review discussed this field’s progress regarding emerging model systems with a focused view on the in vitro platforms. The inadequacy of currently available models and their implications on existing studies also analyzed. The need for a conceptual and experimental leap toward a human-relevant in vitro custom-built platform for studying tumor-macrophage crosstalk is acknowledged.

Cytomegalovirus and Epstein-Barr Infections: Prevalence and Impact on Patients with Hematological Diseases

Cytomegalovirus (CMV) and Epstein-Barr virus (EBV) infections are widely distributed throughout the world. EBV is linked to various hematological and autoimmune disorders whereas CMV might play important role in the progression of chronic hematological diseases, such as hemoglobinopathies, lymphomas, myelomas, hemophilia, and aplastic and sickle cell anemia. Both viruses produce a viral homolog of human interleukin-10 that can cause general suppression of immune response, increasing susceptibility to other infections. These viruses can remain latent in the host cells and be reactivated when the host immune system is compromised. Studies showing the impact of CMV and EBV infections on hematological disorders are scarce and unclear in the context of coinfection. This review intends to present the biology, prevalence, and impact of CMV and EBV infections in patients with hematological diseases.

IgG glycosylation in autoimmune diseases

Immunoglobulin G (IgG) is the most abundant glycoprotein in human serum. All IgG subclasses have a single-conserved N-linked glycosylation site at Asn297 of the heavy chain and 10–30% of IgGs are N-glycosylated also in a Fab region. N-glycans of Fc are sialylated and fucosylated biantennary complex-type structures. Glycosylation plays a key role in antibody function, and IgG N-glycans are essential for the proper activity of the immune system. Fc glycans are important for IgG effector functions, whereas Fab oligosaccharides modulate antigen binding. Glycosylation changes of IgG are associated with the development of various human diseases, including autoimmune states. The modification of one sugar moiety in N-glycan structure may result in the stimulation or suppression of immune response. The lack of core fucose leads to the enhancement of pro-inflammatory activity, whereas an increase of sialylation determines immunosuppressive properties of IgG. The contribution of IgG Fc glycosylation changes has been demonstrated in the pathogenesis of rheumatoid arthritis, lupus erythematosus and Crohn’s disease. A decrease in IgG galactosylation and sialylation, found in these diseases, activates effector cells and triggers inflammatory reactions. A detailed analysis of changes in IgG glycosylation and their effects on the development of autoimmune diseases is important in the treatment of these diseases. IgGs with modified α2,6-sialylation are used as therapeutic antibodies with anti-inflammatory properties. Numerous studies on IgG glycosylation have provided evidence of the role of this post-translational modification in the proper functioning of antibodies and the importance of changes in the structure of IgG glycans, mainly incomplete galactosylation and desialylation, in the pathogenesis of many diseases. The continuation of these studies may contribute to explaining the mechanisms of autoimmunity that is still poorly understood.