The role of cytokines in the immunity development at helminthiasis

2016 ◽  
Vol 3 (4) ◽  
pp. 521-526
Author(s):  
Гришина ◽  
E. Grishina
Keyword(s):  
T Cells ◽  
Defense Mechanism ◽  
Cytotoxic T Cells ◽  
Relationship Building ◽  
Practical Implementation ◽  
Local Immunity ◽  
Effector Cells ◽  
Cd8 Cells ◽  
Protection Mechanisms ◽  
Low Efficiency

Intensive development of the parasitic diseases immunology in the past decade allows making a definite conclusion about the features of the immune response formation in helminthiasis and its key problems, such as short duration, low-efficiency and the ability to cause the development of immunopathological processes. Objective of research: The aim of this review was to identify most significant stages of helminthiasis immunogenesis wich can cause its low protective ability, and for which further comprehensive study of modern molecular biologists, geneticists, biochemists, immunologists and parasitologists should be held to clarify the immunopathology induction mechanisms and improve methods of prophylaxis, diagnosis and treatment of these diseases. Results and discussion. Studies have revealed that the main condition for relationship building in the system “parasite-host” is the presence of protection mechanisms in helminths against exposure to the host’s immune system and immunomodulation mechanisms up to the complete immunosuppression in host. Products of helminths vital activity, so-called secretory-excretory products (SEPs), as well as changed in the process of pathogenesis host proteins and cells become a powerful immune stimulus and activate mechanisms for general and local immunity. The following defense mechanism in helminthiasis is the most effective: participation of IgE antibodies class and IgG2 subclass which play a major role in the activation of cell adhesive activity; influence of cytotoxic T cells (T killer cells, CD8+ -cells); involvement of macrophages, activated with T-cells; work of induced effector cells (eosinophils, neutrophils, mast cells, platelets, etc.), and the results of natural killer (NK) and regulating Treg- lymphocyte population (CD4 + CD25 + -cells) activity. It was shown that helminthiasis is accompanied by oxidative stress, which is characterized by decreased activity of catalase, superoxide dismutase, and an increase of lipid peroxidation products, which may cause primary DNA damage underlying in gene and chromosomal mutations that is shown in prior studies. Parasites metabolites have a cytotoxic effect on somatic, generative and immune cells of host, causing the increase of apoptotic cells among them. Theoretical significance of the data on identification problems of helminthiases immunology is undoubted. Its practical implementation offers the significant increase in the effectiveness of helminthiasis prevention and control.

scholarly journals Diagnostic and pathogenic features of calcifying pseudoneoplasm of the neuraxis

2021 ◽  
Vol 48 (s1) ◽  
pp. S3-S3
Author(s):  
K Yang ◽  
K Reddy ◽  
BH Wang ◽  
A Cenic ◽  
LC Ang ◽  
...  
Keyword(s):  
T Cells ◽  
Cytotoxic T Cells ◽  
Giant Cells ◽  
List Type ◽  
Neurofilament Protein ◽  
Fibrous Stroma ◽  
Cd8 Cells ◽  
Immunohistochemical Markers ◽  
Spinal Epidural ◽  
Age Range

Calcifying pseudoneoplasm of the neuraxis (CAPNON) is a rare tumefactive lesion with unclear pathogenesis. It is diagnosed by pathological findings of the typical histological features that include granular amorphous cores with palisading spindle to epithelioid cells, variable fibrous stroma, foreign-body reaction with giant cells, and calcification/ossification occasionally with psammoma bodies. However, its histopathology may be variable and currently immunohistochemistry plays a limited role in its diagnosis and understanding the pathogenesis. In this study, we examined 6 cases of CAPNONs including 3 intracranial and 3 spinal epidural lesions (age range: 59–69 years; 3 males and 3 females). Immunohistochemistry revealed that all CAPNON cores contain abundant positive deposits of neurofilament protein (NFP), which was supported by electron microscopy finding of filaments (8–13 nm in diameter). In comparison, no NFP positivity was found in 5 psammomatous/metaplastic meningiomas or 7 intervertebral tissue lesions with calcification/ossification. In addition, CAPNON cellular areas showed variable numbers of CD8+ cytotoxic T-cells with less CD4+ T-cells and a decreased ratio of CD4/CD8+ cells, versus the intervertebral tissue lesions without CD8+ or CD4+ cells. Our findings suggest that NFP may be a principal constituent of CAPNONs, and thus involved in the pathogenesis of CAPNON. Given the decreased CD4/CD8 ratio, the pathogenic process of CAPNON is possibly immune- mediated.LEARNING OBJECTIVESThe presentation will enable the learner to: 1.Discuss histopathological features of calcifying pseudoneoplasm of the neuraxis (CAPNON) with variation of non-core components.2.Explore diagnostic and pathogenic roles of immunohistochemical markers including neurofilament protein and CD4/CD8 in CAPNON.

scholarly journals Keratinocyte growth factor enhances DNA plasmid tumor vaccine responses after murine allogeneic bone marrow transplantation

Blood ◽  
2009 ◽  
Vol 113 (7) ◽  
pp. 1574-1580 ◽  
Author(s):  
Robert R. Jenq ◽  
Christopher G. King ◽  
Christine Volk ◽  
David Suh ◽  
Odette M. Smith ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
T Cell ◽  
Keratinocyte Growth Factor ◽  
Allogeneic Bone Marrow Transplantation ◽  
Allogeneic Bone ◽  
Effector Cells ◽  
Cd8 Cells ◽  
T Cell Reconstitution ◽  
Dna Plasmid

Abstract Keratinocyte growth factor (KGF), which is given exogenously to allogeneic bone marrow transplantation (allo-BMT) recipients, supports thymic epithelial cells and increases thymic output of naive T cells. Here, we demonstrate that this improved T-cell reconstitution leads to enhanced responses to DNA plasmid tumor vaccination. Tumor-bearing mice treated with KGF and DNA vaccination have improved long-term survival and decreased tumor burden after allo-BMT. When assayed before vaccination, KGF-treated allo-BMT recipients have increased numbers of peripheral T cells, including CD8+ T cells with vaccine-recognition potential. In response to vaccination, KGF-treated allo-BMT recipients, compared with control subjects, generate increased numbers of tumor-specific CD8+ cells, as well as increased numbers of CD8+ cells producing interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α). We also found unanticipated benefits to antitumor immunity with the administration of KGF. KGF-treated allo-BMT recipients have an improved ratio of T effector cells to regulatory T cells, a larger fraction of effector cells that display a central memory phenotype, and effector cells that are derived from a broader T-cell–receptor repertoire. In conclusion, our data suggest that KGF can function as a potent vaccine adjuvant after allo-BMT through its effects on posttransplantation T-cell reconstitution.

scholarly journals Participation of the H-2 antigens of tumor cells in their lysis by syngeneic T cells.

1976 ◽  
Vol 143 (3) ◽  
pp. 601-614 ◽  
Author(s):  
J W Schrader ◽  
G M Edelman
Keyword(s):  
T Cells ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Target Cell ◽  
Cytotoxic T Cells ◽  
Hybrid Origin ◽  
Target Cells ◽  
Cytotoxic Lymphocytes ◽  
Effector Cells

Cytotoxic T lymphocytes were generated in vitro against H-2 compatible or syngeneic tumor cells. In vitro cytotoxic activity was inhibited by specific anti-H2 sera, suggesting that H-2 antigens are involved in cell lysis. Two observations directly demonstrated the participation of the H-2 antigens on the tumor cells in their lysis by H-2-compatible T cells. First, coating of the H-2 antigens on the target tumor cell reduced the number of cells lysed on subsequent exposure to cytotoxic T cells. Second, when cytotoxic T cells were activated against an H-2 compatible tumor and assayed against an H-2-incompatible tumor, anti-H-2 serum that could bind to the target cell, but not to the cytotoxic lymphocyte, inhibited lysis. H-2 antigens were also shown to be present on the cytotoxic lymphocytes. Specific antisera reacting with these H-2 antigens, but not those of the target cell, failed to inhibit lysis when small numbers of effector cells were assayed against H-2-incompatible target cells or when effector cells of F1-hybrid origin and bearing two H-2 haplotypes were assayed against a tumor cell of one of the parental strains. These findings suggest that it is the H-2 antigens on the tumor cell and not those on the cytotoxic lymphocytes that are important in cell-mediated lysis of H-2-compatible tumor cells.

Thyroid status regulates tumor microenvironment delineating breast cancer fate

2021 ◽  
Author(s):  
Helena Andrea Sterle ◽  
Ximena Hildebrandt ◽  
Matías Valenzuela Álvarez ◽  
María Alejandra Paulazo ◽  
Luciana Mariel Gutierrez ◽  
...  
Keyword(s):  
Breast Cancer ◽  
T Cells ◽  
Tumor Microenvironment ◽  
Lung Metastasis ◽  
Cytotoxic T Cells ◽  
Suppressor Cells ◽  
Thyroid Status ◽  
Cd8 Cells ◽  
Regulatory T Lymphocytes ◽  
Starting Point

The patient’s hormonal context plays a crucial role in the outcome of cancer. However, the association between thyroid disease and breast cancer risk remains unclear. We evaluated the effect of thyroid status on breast cancer growth and dissemination in an immunocompetent mouse model. For this, hyperthyroid and hypothyroid Balb/c mice were orthotopically inoculated with triple negative breast cancer 4T1 cells. Tumors from hyperthyroid mice showed increased growth rate and an immunosuppressive tumor microenvironment, characterized by increased IL-10 levels and decreased percentage of activated cytotoxic T cells. On the other hand, a delayed tumor growth in hypothyroid animals was associated with increased tumor infiltration of activated CD8+ cells and a high IFNγ/IL-10 ratio. Paradoxically, hypothyroid mice developed a higher number of lung metastasis than hyperthyroid animals. This was related to an increased secretion of tumor CCL2 and an immunosuppressive systemic environment, with increased proportion of regulatory T cells and IL-10 levels in spleens. A lower number of lung metastasis in hyperthyroid mice was related to the reduced presence of mesenchymal stem cells in tumors and metastatic sites. These animals also exhibited decreased percentages of regulatory T lymphocytes and myeloid-derived suppressor cells in spleens, but increased activated CD8+ cells and IFNγ/IL-10 ratio. Therefore, thyroid hormones modulate the cellular and cytokine content of the breast tumor microenvironment. The better understanding of the mechanisms involved in these effects could be a starting point for the discovery of new therapeutic targets for breast cancer.

scholarly journals Human macrophage inflammatory protein alpha (MIP-1 alpha) and MIP-1 beta chemokines attract distinct populations of lymphocytes.

1993 ◽  
Vol 177 (6) ◽  
pp. 1821-1826 ◽  
Author(s):  
T J Schall ◽  
K Bacon ◽  
R D Camp ◽  
J W Kaspari ◽  
D V Goeddel
Keyword(s):  
T Cells ◽  
B Cells ◽  
Cytotoxic T Cells ◽  
Human Macrophage ◽  
Immune Effector ◽  
Effector Cells ◽  
Inflammatory Protein ◽  
And Migration ◽  
Macrophage Inflammatory Protein

Lymphocyte trafficking is an essential process in immune and inflammatory functions which can be thought to contain at least two main components: adhesion and migration. Whereas adhesion molecules such as the selections are known to mediate the homing of leukocytes from the blood to the endothelium, the chemoattractant substances responsible for the migration of specific subsets of lymphocytes to sites of infection or inflammation are largely unknown. Here we show that two molecules in the chemokine (for chemoattractant cytokine) superfamily, human macrophage inflammatory protein 1 alpha (MIP-1 alpha) and MIP-1 beta, do not share identical attractant activities for lymphocyte subpopulations. When analyzed in vitro in microchemotaxis experiments, HuMIP-1 beta tends to attract CD4+ T lymphocytes, with some preference for T cells of the naive (CD45RA) phenotype. HuMIP-1 alpha, when tested in parallel with HuMIP-1 beta, is a more potent lymphocyte chemoattractant with a broader range of concentration-dependent chemoattractant specificities. HuMIP-1 alpha at a concentration of 100 pg/ml attracts B cells and cytotoxic T cells, whereas at higher concentrations (10 ng/ml), the migration of these cells appears diminished, and the migration of CD4+ T cells is enhanced. Thus, in this assay system, HuMIP-1 alpha and -1 beta have differential attractant activities for subsets of immune effector cells, with HuMIP-1 alpha having greater effects than HuMIP-1 beta, particularly on B cells.

The Role of ERK5 Signaling in Tolerance Induction by Veto CTLs.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3302-3302
Author(s):  
Shlomit Reich-Zeliger ◽  
Tamar Hanoch ◽  
Rony Seger ◽  
Yair Reisner
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
Cellular Systems ◽  
Class I ◽  
Spleen Cells ◽  
Effector Cells ◽  
Cd8 Cells ◽  
Veto Cells ◽  
Specific Inhibitors

Abstract Several bone marrow cells and lymphocyte subpopulations, known as ‘veto cells’, were shown to induce transplantation tolerance across major histocompatibility antigens. Recently, it has been suggested that anti-3rd party CTLs depleted of alloreactivity against the host are endowed with marked veto activity and can facilitate bone marrow allografting. The veto mechanism is still obscure. While early studies emphasized the role of CD8 mediated apoptosis, we showed that the veto activity of anti-3rd party CD8+ CTLs is dependent upon the simultaneous expression of both CD8 and FasL. Thus, it seems that although Fas is upregulated on the effector T cells upon engagement of their TCR by class I of the veto cells, the presence of FasL on the veto cells cannot result in apoptosis of the effector cells unless CD8 on the veto cells is available and can interact with class 1 on the effector cells. Thus, the interaction of CD8 on the veto cells with class I on the effector cells seems to be associated with an increased susceptability of the effector cells to FasL killing. To further delineate the mechanism of the veto effect we have now studied the role of different signaling pathways using specific inhibitors. Spleen CD8 T cells from 2C mice (H2b) bearing TCR transgene directed against (H2d) were used as effector cells and anti FVB (H2q, third party) CTLs generated from Balb/c spleen cells (H2d) were used as veto cells. The addition of the latter cells to MLR of 2C against Balb/c (H2d) simulators, leads to deletion of the 2C effector CD8 cells within 72 hrs. Deletion monitored by FACS analysis of cells stained with anti-TCR transgene antibody (1B2+) revealed reduction from 46%±11% 1B2+CD8+ cells to 6%±3% 1B2+CD8+ cells in 6 different experiments. In contrast, veto CTLs generated from SJL (H2s) spleen cells that do not display the H2 recognized by the 2C effector cells, did not result in a significant deletion of the effector cells (42%±12% 1B2+CD8+ cells in 6 different experiments). The specific deletion exhibited by veto CTLs of Balb/c origin, can be inhibited by MEK1/2/5 inhibitors such as U0126, reducing the veto activity from 85.5%±7% to 16%±14% in 6 different experiments. The effective concentration of U0126 was relatively high (10μM), and lower concentration of this drug (1μM) had no response, indicating a potential involvement of the MEK5/ERK5 cascade rather than the MEK1/2-ERK1/2 cascade, in the veto effect. In addition, no inhibition of veto activity could be found with specific inhibitors of other signaling molecules such as JNK, P38, PI3K or PKC. Considering that Fas expression on the effector cells is critical for the veto activity, it is interesting that the ERK inhibitor didn’t affect the level of Fas on the effectors (93%±3% of 1B2+CD8+ upregulate FAS in the presence of U0126 in 7 different experiments). Also, this inhibition is not likely mediated by affecting the veto CTLs, as pretreatment of the latter cells with ERK inhibitor didn’t diminish the veto effect. The pro-apoptotic effects of MEK5-ERK5 cascade in this system is intriguing because these kinases are usually thought to promote proliferation and survival in most cellular systems. Therefore, the veto cells exhibit a unique signaling system, which utilizes ERK5 cascade to induce apoptosis. Further studies are directed at the potential links between the ERK5 cascade, the Fas system and the rest of the apoptotic machinery.

scholarly journals Specificity of cytotoxicity T cells directed to influenza virus hemagglutinin.

1979 ◽  
Vol 149 (4) ◽  
pp. 856-869 ◽  
Author(s):  
T J Braciale
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cytotoxic T Cells ◽  
Type A ◽  
Cross Reactivity ◽  
Cytotoxic T Cell ◽  
Target Cells ◽  
Effector Cells ◽  
Cell Induction

Purified type A influenza viral hemagglutinin stimulates an in vitro cell-mediated cytotoxic cell response that exhibits a high degree of specificity for the immunizing hemagglutinin. The response magnitude is proportional to the hemagglutinin dose used for stimulation. The lytic activity of the effector cells is H-2 restricted. Analysis of the specificity of the response indicated that these cytotoxic T cells readily distinguish target cells expressing serologically unrelated hemagglutinin from target cells bearing hemagglutinins serologically related to the stimulating hemagglutinin. Further analysis of the fine specificity of cytotoxic T-cell recognition with serologically cross-reactive type A influenza hemagglutinins revealed a hierarchy of cross-reactivity among these hemagglutinins that was the converse of the serologic hierarchy. These results are discussed in terms of possible differences and similarities in the specificity repertoire of cytotoxic T cells and antibodies. Possible implications of these findings from the standpoint of cytotoxic T-cell induction are also discussed.

scholarly journals CD73 Ectonucleotidase Restrains CD8+ T Cell Metabolic Fitness and Anti-tumoral Activity

2021 ◽  
Vol 9 ◽  
Author(s):  
Pedro Briceño ◽  
Elizabeth Rivas-Yañez ◽  
Mariana V. Rosemblatt ◽  
Brian Parra-Tello ◽  
Paula Farías ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd8 T Cells ◽  
Cytotoxic T Cells ◽  
Cd8 T Cell ◽  
Tumor Burden ◽  
Effector Cells ◽  
Cd73 Expression ◽  
Metabolic Fitness

CD39 and CD73 are ectoenzymes that dephosphorylate ATP into its metabolites; ADP, AMP, and adenosine, and thus are considered instrumental in the development of immunosuppressive microenvironments. We have previously shown that within the CD8+ T cell population, naïve and memory cells express the CD73 ectonucleotidase, while terminally differentiated effector cells are devoid of this enzyme. This evidence suggests that adenosine might exert an autocrine effect on CD8+ T cells during T cell differentiation. To study the possible role of CD73 and adenosine during this process, we compared the expression of the adenosinergic signaling components, the phenotype, and the functional properties between CD73-deficient and WT CD8+ T cells. Upon activation, we observed an upregulation of CD73 expression in CD8+ T cells along with an upregulation of the adenosine A2A receptor. Interestingly, when we differentiated CD8+ T cells to Tc1 cells in vitro, we observed that these cells produce adenosine and that CD73-deficient cells present a higher cytotoxic potential evidenced by an increase in IFN-γ, TNF-α, and granzyme B production. Moreover, CD73-deficient cells presented a increased glucose uptake and higher mitochondrial respiration, indicating that this ectonucleotidase restrict the mitochondrial capacity in CD8+ T cells. In agreement, when adoptively transferred, antigen-specific CD73-deficient CD8+ T cells were more effective in reducing the tumor burden in B16.OVA melanoma-bearing mice and presented lower levels of exhaustion markers than wild type cells. All these data suggest an autocrine effect of CD73-mediated adenosine production, limiting differentiation and cytotoxic T cells’ metabolic fitness.

A study of the immune infiltrate and patient outcomes in esophageal cancer

2020 ◽  
Author(s):  
Melissa J Conroy ◽  
Susan A Kennedy ◽  
Suzanne L Doyle ◽  
Brian Hayes ◽  
Maria Kavanagh ◽  
...  
Keyword(s):  
T Cells ◽  
Esophageal Cancer ◽  
Patient Outcomes ◽  
Immune Cell ◽  
Cytotoxic T Cells ◽  
Tissue Microarrays ◽  
Stromal Compartment ◽  
Cancer Subtypes ◽  
Cd8 Cells ◽  
Esophageal Tumors

Abstract Objectives Cancer patient outcomes and selection for novel therapies are heavily influenced by the immune contexture of the tumor microenvironment. Esophageal cancer is associated with poor outcomes. In contrast to colorectal cancer, where the immunoscore is increasingly used in prognostic staging, little is known about the immune cell populations in esophageal adenocarcinoma (EAC) and esophageal squamous cell carcinoma (SCC), and their clinical significance. Methods Tissue microarrays were constructed from resected tumor tissue of 72 EAC patients and 23 SCC patients. Immunohistochemical staining of CD3, CD8, CD56, CD68, CD45RO, CD69, IFN-γ, IL-10, IL-4, IL-17, TGF-β, FOXP3 and CD107a was performed. Positivity was examined in both the stromal and epithelial compartments. Statistical analysis was performed to identify differences in immune cell infiltration and functional phenotypes between cancer subtypes and tissue compartments. Results This study identified that esophageal tumors are enriched with CD45RO+ and CD8+ cells and such positivity is significantly higher in SCC compared with EAC. Furthermore, the expression of CD45RO positively correlates with that of CD8 within the tumors of both patient cohorts, suggesting a dominance of memory cytotoxic T cells. This is supported by strong positivity of degranulation marker CD107a in the stromal compartment of EAC and SCC tumors. Cytokine staining revealed a mixed pro- and anti-inflammatory profile within EAC tumors. Conclusions Esophageal tumors are enriched with memory cytotoxic T cells. Applying these measurements to a larger cohort will ascertain the clinical utility of assessing specific lymphocyte infiltrates in EAC and SCC tumors with regards to future immunotherapy use, patient prognosis and outcomes.

Redirection of CMV Specific CTL towards B-CLL Via CD20 Targeted HLA/CMV Complexes.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 449-449 ◽  
Author(s):  
Rogier Mous ◽  
Philip Savage Savage ◽  
Ester BM Remmerswaal ◽  
Rene A.W. van Lier ◽  
Eric Eldering ◽  
...  
Keyword(s):  
T Cells ◽  
B Cell ◽  
Immunological Synapse ◽  
Ex Vivo ◽  
Cytotoxic T Cells ◽  
Interferon Γ ◽  
Lymphocytic Leukemia ◽  
Viral Immunity ◽  
Single Chain ◽  
Effector Cells

Abstract Because B cell chronic lymphocytic leukemia (B-CLL) can not be cured with current therapies, but in general has a slow progression and rather long median survival, it is considered an attractive candidate for active T cell mediated immunotherapy. However B-CLL cells have poor antigen presenting capacity because they express low levels of co-stimulatory molecules. Moreover, most immunotherapeutic strategies require knowledge of the eliciting tumor antigen and/or ex vivo manipulation of patient cells. To circumvent these drawbacks we aim to redirect existing viral immunity towards B-CLL. Previously, we have shown that in patients with B-CLL considerably expanded numbers of cytomegalovirus (CMV)-specific CD45RA+CD27 CD8+ cytotoxic T cells are present (W. Mackus et al. Blood2003; 102:1057). These cells are potent cytotoxic effector cells when directed against B-CLL cells loaded with CMV peptide (A.Kater et al. Br.J. Haematol.2004; 126:512). In the current study, we apply a novel bridging reagent to redirect CMV-specific CTL to specifically target B-CLL. The targeting complex is composed of a streptavidin fused anti-CD20 single chain variable fragment (scFv) in combination with biotinylated MHC class I molecules containing CMV pp65 peptide (HLA/CMV). We demonstrate that this complex is stable on the cell surface for ≥24 hours, and that B-CLL cells coated with this CD20-HLA/CMV complex can be lysed by autologous CMV-specific CD8+ CTL with similar efficiency as B-CLL cells directly loaded with CMV-peptide. Killing occurs at scFv CD20 concentrations of ≥100 ng ml−1 and HLA/CMV concentrations of ≥20 ng ml−1. Lysis of CD20-HLA/CMV complex coated CLL cells could not be blocked by anti-LFA1 antibodies, in contrast to B-CLL cells directly loaded with CMV-peptide, indicating a different immunological synapse. HLA-A2 positive B-CLL cells coated with HLA-B7 /CMV complexes were only lysed by HLA-B7 positive CMV-specific CTL, whereas HLA-A2/CMV complex targeted HLA-A2 positive B-CLL cells were unaffected by HLA-B7 positive CMV specific CTL, proving HLA restriction of the killing.. Furthermore, CD20-HLA/CMV complex coated B-CLL cells induce both proliferation and cytokine production (interferon γ, tumor necrosis factor α, and macrophage inflammatory protein-1 β) in CMV-specific CD8+ T cells. Thus, CD20-HLA/CMV complexes elicit both immune activation and direct cytotoxicity towards B-CLL cells. The findings of our study constitute a necessary step towards possible application of CD20-HLA/CMV complexes for immunotherapy of B cell malignancies. It is obvious that this recently recognized capacity to redirect existing antiviral immunity towards tumor cells has a utility in cancer immunotherapy far beyond CMV and B-CLL.

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