Immune profile of tumor and chemotherapy

2018 ◽  
Vol 3 (2) ◽  
pp. 54
Author(s):  
Bakulesh Khamar
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Immune Cells ◽  
Prognostic Value ◽  
Cell Mediated Immunity ◽  
Cell Mediated Immune Response ◽  
Current Classification ◽  
Immunosuppressive Cells

<p>Chemotherapy works through its activity on cancer cells. It generally suppresses cell-mediated immunity but also improves cell-mediated immune response by making tumor cells vulnerable to killing by cell-mediated immune responses as well as through its action on immunostimulant and immunosuppressive cells. Outcome of chemotherapy seems to be dependent on baseline tumor-infiltrating immune cells (TII) as well as changes in TII following chemotherapy in varieties of tumors. Evaluation of density and site of two TII is done in immunoscore. It is a better marker than evaluation of a single TII. Evaluation of TII can have prognostic and predictive value and can help in the better stratifying prognostic value of current classification.</p>

scholarly journals Semaphorin Signaling in Cancer-Associated Inflammation

2019 ◽  
Vol 20 (2) ◽  
pp. 377 ◽  
Author(s):  
Giulia Franzolin ◽  
Luca Tamagnone
Keyword(s):  
Immune Response ◽  
Tumor Microenvironment ◽  
Cancer Cells ◽  
Disease Progression ◽  
Tumor Cells ◽  
Cross Talk ◽  
Immune Cells ◽  
Major Element ◽  
Inflammatory Cells ◽  
Anti Cancer

The inflammatory and immune response elicited by the growth of cancer cells is a major element conditioning the tumor microenvironment, impinging on disease progression and patients’ prognosis. Semaphorin receptors are widely expressed in inflammatory cells, and their ligands are provided by tumor cells, featuring an intense signaling cross-talk at local and systemic levels. Moreover, diverse semaphorins control both cells of the innate and the antigen-specific immunity. Notably, semaphorin signals acting as inhibitors of anti-cancer immune response are often dysregulated in human tumors, and may represent potential therapeutic targets. In this mini-review, we provide a survey of the best known semaphorin regulators of inflammatory and immune cells, and discuss their functional impact in the tumor microenvironment.

scholarly journals Photodynamic Therapy Using a New Folate Receptor-Targeted Photosensitizer on Peritoneal Ovarian Cancer Cells Induces the Release of Extracellular Vesicles with Immunoactivating Properties

2020 ◽  
Vol 9 (4) ◽  
pp. 1185 ◽  
Author(s):  
Martha Baydoun ◽  
Olivier Moralès ◽  
Céline Frochot ◽  
Colombeau Ludovic ◽  
Bertrand Leroux ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Immune Response ◽  
Photodynamic Therapy ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Extracellular Vesicles ◽  
Immune Cells ◽  
Surgical Techniques ◽  
Ovarian Cancer Cells ◽  
The Impact

Often discovered at an advanced stage, ovarian cancer progresses to peritoneal carcinoma, which corresponds to the invasion of the serosa by multiple tumor implants. The current treatment is based on the combination of chemotherapy and tumor cytoreduction surgery. Despite the progress and standardization of surgical techniques combined with effective chemotherapy, post-treatment recurrences affect more than 60% of women in remission. Photodynamic therapy (PDT) has been particularly indicated for the treatment of superficial lesions on large surfaces and appears to be a relevant candidate for the treatment of microscopic intraperitoneal lesions and non-visible lesions. However, the impact of this therapy on immune cells remains unclear. Hence, the objective of this study is to validate the efficacy of a new photosensitizer [pyropheophorbide a-polyethylene glycol-folic acid (PS)] on human ovarian cancer cells and to assess the impact of the secretome of PDT-treated cells on human peripheral blood mononuclear cells (PBMC). We show that PS, upon illumination, can induce cell death of different ovarian tumor cells. Furthermore, PDT using this new PS seems to favor activation of the immune response by inducing the secretion of effective cytokines and inhibiting the pro-inflammatory and immunosuppressive ones, as well as releasing extracellular vesicles (EVs) prone to activating immune cells. Finally, we show that PDT can activate CD4+ and CD8+ T cells, resulting in a potential immunostimulating process. The results of this pilot study therefore indicate that PS-PDT treatment may not only be effective in rapidly and directly destroying target tumor cells but also promote the activation of an effective immune response; notably, by EVs. These data thus open up good prospects for the treatment of micrometastases of intraperitoneal ovarian carcinosis which are currently inoperable.

scholarly journals Combining Oncolytic Viruses and Small Molecule Therapeutics: Mutual Benefits

Cancers ◽  
2021 ◽  
Vol 13 (14) ◽  
pp. 3386
Author(s):  
Bart Spiesschaert ◽  
Katharina Angerer ◽  
John Park ◽  
Guido Wollmann
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Tumor Cells ◽  
Small Molecule ◽  
Antiviral Immunity ◽  
Oncolytic Viruses ◽  
Antitumor Immune Response ◽  
Antiviral Responses ◽  
Small Molecule Therapeutics ◽  
Immunosuppressive Factors

The focus of treating cancer with oncolytic viruses (OVs) has increasingly shifted towards achieving efficacy through the induction and augmentation of an antitumor immune response. However, innate antiviral responses can limit the activity of many OVs within the tumor and several immunosuppressive factors can hamper any subsequent antitumor immune responses. In recent decades, numerous small molecule compounds that either inhibit the immunosuppressive features of tumor cells or antagonize antiviral immunity have been developed and tested for. Here we comprehensively review small molecule compounds that can achieve therapeutic synergy with OVs. We also elaborate on the mechanisms by which these treatments elicit anti-tumor effects as monotherapies and how these complement OV treatment.

scholarly journals The immune response of T cells and therapeutic targets related to regulating the levels of T helper cells after ischaemic stroke

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Tian-Yu Lei ◽  
Ying-Ze Ye ◽  
Xi-Qun Zhu ◽  
Daniel Smerin ◽  
Li-Juan Gu ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Immune System ◽  
Immune Responses ◽  
Ischaemic Stroke ◽  
Immune Cells ◽  
Tissue Injury ◽  
Recovery Period ◽  
Vital Functions ◽  
Anti Inflammatory

AbstractThrough considerable effort in research and clinical studies, the immune system has been identified as a participant in the onset and progression of brain injury after ischaemic stroke. Due to the involvement of all types of immune cells, the roles of the immune system in stroke pathology and associated effects are complicated. Past research concentrated on the functions of monocytes and neutrophils in the pathogenesis of ischaemic stroke and tried to demonstrate the mechanisms of tissue injury and protection involving these immune cells. Within the past several years, an increasing number of studies have elucidated the vital functions of T cells in the innate and adaptive immune responses in both the acute and chronic phases of ischaemic stroke. Recently, the phenotypes of T cells with proinflammatory or anti-inflammatory function have been demonstrated in detail. T cells with distinctive phenotypes can also influence cerebral inflammation through various pathways, such as regulating the immune response, interacting with brain-resident immune cells and modulating neurogenesis and angiogenesis during different phases following stroke. In view of the limited treatment options available following stroke other than tissue plasminogen activator therapy, understanding the function of immune responses, especially T cell responses, in the post-stroke recovery period can provide a new therapeutic direction. Here, we discuss the different functions and temporal evolution of T cells with different phenotypes during the acute and chronic phases of ischaemic stroke. We suggest that modulating the balance between the proinflammatory and anti-inflammatory functions of T cells with distinct phenotypes may become a potential therapeutic approach that reduces the mortality and improves the functional outcomes and prognosis of patients suffering from ischaemic stroke.

scholarly journals TAM Receptor Inhibition–Implications for Cancer and the Immune System

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1195
Author(s):  
Pia Aehnlich ◽  
Richard Morgan Powell ◽  
Marlies J. W. Peeters ◽  
Anne Rahbech ◽  
Per thor Straten
Keyword(s):  
T Cells ◽  
Immune Responses ◽  
Cancer Cells ◽  
Immune Cells ◽  
Tyrosine Kinases ◽  
Apoptotic Cell ◽  
Receptor Activation ◽  
Mouse Tumor ◽  
Oncogenic Signaling ◽  
Tam Receptors

Tyro3, Axl and MerTK (TAM) receptors are receptor tyrosine kinases which play important roles in efferocytosis and in the balancing of immune responses and inflammation. TAM receptor activation is induced upon binding of the ligands protein S (Pros1) or growth arrest-specific protein 6 (Gas6) which act as bridging molecules for binding of phosphatidyl serine (PtdSer) exposed on apoptotic cell membranes. Upon clearance of apoptotic cell material, TAM receptor activation on innate cells suppresses proinflammatory functions, thereby ensuring the immunologically silent removal of apoptotic material in the absence of deleterious immune responses. However, in T cells, MerTK signaling is costimulatory and promotes activation and functional output of the cell. MerTK and Axl are also aberrantly expressed in a range of both hematological and solid tumor malignancies, including breast, lung, melanoma and acute myeloid leukemia, where they have a role in oncogenic signaling. Consequently, TAM receptors are being investigated as therapeutic targets using small molecule inhibitors and have already demonstrated efficacy in mouse tumor models. Thus, inhibition of TAM signaling in cancer cells could have therapeutic value but given the opposing roles of TAM signaling in innate cells and T cells, TAM inhibition could also jeopardize anticancer immune responses. This conflict is discussed in this review, describing the effects of TAM inhibition on cancer cells as well as immune cells, while also examining the intricate interplay of cancer and immune cells in the tumor microenvironment.

scholarly journals Dual-Wavelength Photosensitive Nano-in-Micro Scaffold Regulates Innate and Adaptive Immune Responses for Osteogenesis

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Qin Zhao ◽  
Miusi Shi ◽  
Chengcheng Yin ◽  
Zifan Zhao ◽  
Jinglun Zhang ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Immune Cells ◽  
Inflammatory Responses ◽  
Macrophage Polarization ◽  
T Cell Response ◽  
Dual Wavelength ◽  
M2 Macrophage ◽  
Adaptive Immune Responses ◽  
Adaptive Immune

AbstractThe immune response of a biomaterial determines its osteoinductive effect. Although the mechanisms by which some immune cells promote regeneration have been revealed, the biomaterial-induced immune response is a dynamic process involving multiple cells. Currently, it is challenging to accurately regulate the innate and adaptive immune responses to promote osteoinduction in biomaterials. Herein, we investigated the roles of macrophages and dendritic cells (DCs) during the osteoinduction of biphasic calcium phosphate (BCP) scaffolds. We found that osteoinductive BCP directed M2 macrophage polarization and inhibited DC maturation, resulting in low T cell response and efficient osteogenesis. Accordingly, a dual-targeting nano-in-micro scaffold (BCP loaded with gold nanocage, BCP-GNC) was designed to regulate the immune responses of macrophages and DCs. Through a dual-wavelength photosensitive switch, BCP-GNC releases interleukin-4 in the early stage of osteoinduction to target M2 macrophages and then releases dexamethasone in the later stage to target immature DCs, creating a desirable inflammatory environment for osteogenesis. This study demonstrates that biomaterials developed to have specific regulatory capacities for immune cells can be used to control the early inflammatory responses of implanted materials and induce osteogenesis.

scholarly journals High Expression of Pd-1 in Circulating Cells of Patients With Advanced Colorectal Cancer Receiving Adjuvant Therapy

2020 ◽  
Vol 19 ◽  
pp. 153303382096944
Author(s):  
Muhammed A. Bakhrebah ◽  
Mohammad Nasrullah ◽  
Wesam H. Abdulaal ◽  
Mohammed A. Hassan ◽  
Halima Siddiqui ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Immune Response ◽  
Adjuvant Therapy ◽  
Tumor Cells ◽  
Immune Cells ◽  
Human Leukocyte ◽  
Genetic Alterations ◽  
Programmed Death ◽  
Programmed Death 1 ◽  
Cancer Types

Among all cancer types, colorectal cancer is the third most common in men and the second most common in women globally. Generally, the risk of colorectal cancer increases with age, and colorectal cancer is modulated by various genetic alterations. Alterations in the immune response serve a significant role in the development of colorectal cancer. In primary cancer types, immune cells express a variety of inhibitory molecules that dampen the immune response against tumor cells. Additionally, few reports have demonstrated that classical chemotherapy promotes the immunosuppressive microenvironment in both tissues and immune cells. This study assessed the expression levels of genes using RT-qPCR associated with the immune system, including interferon-γ, programmed death-1, β2-microglobulin, human leukocyte antigen-A, CD3e, CD28 and intracellular adhesion molecule 1, in patients with colorectal cancer, as these genes are known to serve important roles in immune regulation during cancer incidence. Gene expression analysis was performed with the whole blood cells of patients with colorectal cancer and healthy volunteers. Compared with the normal controls, programmed death-1was highly expressed in patients with advanced-stage colorectal cancer. Furthermore, the expression of programmed death-1 was higher in patients receiving adjuvant therapy, which suggests the therapy dampened the immune response against tumor cells. The results of the present study indicate that classical adjuvant therapies, which are currently used for patients with colorectal cancer, should be modulated, and a combination of classical therapy with anti-programmed death-1 antibody should be conducted for improved management of patients with colorectal cancer.

The rôle of cortisol and β-endorphin in the response of the immune system to weaning in lambs

1998 ◽  
Vol 66 (2) ◽  
pp. 397-402 ◽  
Author(s):  
S. M. Rhind ◽  
H. W. Reid ◽  
S. R. McMillen ◽  
G. Palmarini
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Stress Hormone ◽  
Keyhole Limpet Haemocyanin ◽  
Weaning Stress ◽  
Cell Mediated Immune Response ◽  
Acth Treatment ◽  
Induced Changes ◽  
The Relationship

AbstractThe relationship between weaning stress-induced changes in stress hormone profiles and immune function was investigated in groups of 10 lambs immunized against adrenocorticotrophic hormone (ACTH; treatment A) or fi-endorphin (treatment B) to reduce the circulating concentrations of cortisol and fi-endorphin respectively. Control animals (treatment C) were immunized against a porcine thyroglobulin carrier protein. Application of weaning stress was associated with significantly elevated plasma cortisol concentrations but no significant increase in fi-endorphin concentrations in C lambs. Immunization against ACTH suppressed the post-weaning increase in cortisol concentration. This was associated with a transient reduction in the lymphocyte stimulation response to keyhole limpet haemocyanin (KLH) antigen in the A animals but there was no effect on the antibody response or interferon-y production by antigen stimulated lymphocytes. There were no significant effects of immunization against fi-endorphin on the capacity to mount antibody or cell-mediated immune responses. It is concluded that weaning stress-induced increases in cortisol did not inhibit the immune response. Since cortisol concentrations and the cell mediated immune response at 8 days after immunization were positively associated it is concluded that these indices are not independent measures of stress.

scholarly journals Production of Adenosine by Ectonucleotidases: A Key Factor in Tumor Immunoescape

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
François Ghiringhelli ◽  
Mélanie Bruchard ◽  
Fanny Chalmin ◽  
Cédric Rébé
Keyword(s):  
Immune Response ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Stromal Cells ◽  
T Cell Response ◽  
Antitumor Immune Response ◽  
Tumor Bed ◽  
Wide Range ◽  
Key Factor ◽  
The Impact

It is now well known that tumor immunosurveillance contributes to the control of cancer growth. Many mechanisms can be used by cancer cells to avoid the antitumor immune response. One such mechanism relies on the capacity of cancer cells or more generally of the tumor microenvironment to generate adenosine, a major molecule involved in antitumor T cell response suppression. Adenosine is generated by the dephosphorylation of extracellular ATP released by dying tumor cells. The conversion of ATP into adenosine is mediated by ectonucleotidase molecules, namely, CD73 and CD39. These molecules are frequently expressed in the tumor bed by a wide range of cells including tumor cells, regulatory T cells, Th17 cells, myeloid cells, and stromal cells. Recent evidence suggests that targeting adenosine by inhibiting ectonucleotidases may restore the resident antitumor immune response or enhance the efficacy of antitumor therapies. This paper will underline the impact of adenosine and ectonucleotidases on the antitumor response.

scholarly journals 26. Is There a Correlation Between Reactogenicity and Immune Responses of the Adjuvanted Recombinant Zoster Vaccine (RZV)? A Post-hoc Analysis

2021 ◽  
Vol 8 (Supplement_1) ◽  
pp. S136-S136
Author(s):  
Andrea Callegaro ◽  
David O Willer ◽  
Wivine Burny ◽  
Caroline Hervé ◽  
Joon Hyung Kim ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Surrogate Marker ◽  
Cell Mediated Immunity ◽  
Global Score ◽  
Post Dose ◽  
Post Vaccination ◽  
Material Support ◽  
Post Hoc Analysis ◽  
Post Hoc

Abstract Background RZV (GSK) contains the varicella-zoster virus antigen glycoprotein E (gE) and the adjuvant system AS01B that enhances gE-specific immune responses through stimulating innate immunity. AS01B may contribute to the development of transient local or systemic post-vaccination reactions. A hypothesis that the magnitude of those reactions is predictive of immunogenicity and efficacy (i.e., “no pain, no gain”) remains untested. To evaluate potential correlations between RZV’s reactogenicity and immunogenicity in adults aged ≥ 50 years, a post-hoc analysis was conducted using data from 2 large phase 3 studies (NCT01165177, NCT01165229). Methods Reactogenicity was calculated as a single score per symptom (maximum grade recorded over 7 days post-vaccination). A global score obtained by adding each maximum severity for all reported symptoms (multivariate reactogenicity models) and a score for each reactogenicity symptom (univariate reactogenicity models) were estimated. Results The analysis included 904 and 147 RZV recipients with completed post-vaccination symptom diary cards and with anti-gE antibody results or cell-mediated immunity (CMI) results, respectively. The global score of reactogenicity post-dose 2 was significantly associated with anti-gE antibody response (p&lt; 0.001, estimate 0.112) although the absolute antibody increase associated with reactogenicity was minimal (1.29-fold increase), while the association with CMI response was not statistically significant (p=0.073, estimate 0.230). There was a weak, but statistically significant association between gE-specific immune responses and the maximum pain post-dose 2 score (p=0.001, estimate 0.041), irrespective of post-vaccination time. Nevertheless, there are observations of immune responses in participants for whom pain was not reported. Conclusion A weak but statistically significant correlation was found between injection site pain intensity and immune responses in adult RZV recipients aged ≥ 50 years. However, participants reporting no pain were also able to mount a strong immune response, therefore pain cannot be a surrogate marker to inform on the level of immune response or on likelihood of being protected against herpes zoster. Funding GlaxoSmithKline Biologicals SA Disclosures Andrea Callegaro, PhD, GSK group of companies (Employee, Shareholder) David O. Willer, PhD, GSK group of companies (Employee, Other Financial or Material Support, Receive GSK shares as part of employment renumeration) Wivine Burny, PhD, GSK group of companies (Employee) Caroline Hervé, PhD, GSK group of companies (Employee) Joon Hyung Kim, MD, GSK group of companies (Employee, Shareholder) myron J. levin, MD, GSK group of companies (Employee, Research Grant or Support) Toufik Zahaf, PhD, GSK group of companies (Employee, Shareholder) Anthony L. Cunningham, F.A.H.M.S., MD, M.B.B.S., B. Med. Sci. (Hons), F.R.A.C.P., F.R.C.P.A., F.A.S.M., GSK group of companies (Grant/Research Support, Advisor or Review Panel member, Speaker’s Bureau) Arnaud Didierlaurent, PhD, GSK group of companies (Other Financial or Material Support, previous employee until 03/2020)Sanofi (Speaker’s Bureau)

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