Toll-Like Receptors in Chronic Lymphocytic Leukemia

Muzio, Marta; Fonte, Eleonora; Caligaris-Cappio, Federico

doi:10.4084/mjhid.2012.055

Cited by 22 publications

(21 citation statements)

References 94 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Next, the impact of TLR signaling, a pathway with high relevance for CLL growth and progression, on the release of EV was analyzed. 8 To minimize non-CpG-related differences among samples we included only IgHV-mutated cases, which are known to be more indolent than the IgHV-unmutated type of CLL. The specific cargo of vesicles from different CLL subsets and the role of TLR signaling on these CLL subsets remains to be analyzed.…”

Section: Letters To the Editormentioning

confidence: 99%

Extracellular vesicles released from chronic lymphocytic leukemia cells exhibit a disease relevant mRNA signature and transfer mRNA to bystander cells

Reiners¹,

Shatnyeva²,

Vasyutina³

et al. 2016

Haematologica

View full text Add to dashboard Cite

Section: Letters To the Editormentioning

confidence: 99%

Extracellular vesicles released from chronic lymphocytic leukemia cells exhibit a disease relevant mRNA signature and transfer mRNA to bystander cells

Reiners¹,

Shatnyeva²,

Vasyutina³

et al. 2016

Haematologica

View full text Add to dashboard Cite

“…In addition to TLR-7 and TLR-9, CLL cells can also express TLR-1, TLR-2, TLR-6 and TLR-10. Meanwhile, Muzio et al (2012) [29] have studied the full expression profile of mRNA for TLR and signaling molecules in a large group of CLL patients to search for potential differences in specific subsets of patients. CLL cells showed high expression of TLR-7, intermediate expression of TLR-1, TLR-6 and TLR-10 and low expression of TLR-2, TLR-4, TLR-8 and TLR-9 and confirmed that CLL cells express functional TLR-9, similar to normal B lymphocytes.…”

Section: Expression Of Tlrmentioning

confidence: 99%

Quantitative Expression of Toll-Like Receptors TLR-7 and TLR-9 on Peripheral Blood Mononuclear Cells in Leukemias

Morsi¹,

Gharabawy²,

Hamed³

et al. 2016

J Hematol

View full text Add to dashboard Cite

Background: Toll-like receptors (TLRs) are agents of innate and adaptive immunity, involved in tumor activation. The expression and functionality of TLR on leukemic cells have seldom been investigated. The aims of the study were to throw some light on the quantitative expression of TLR-7 and TLR-9 on leukemic cells and to compare it with their expression on mononuclear cells of healthy volunteers.

show abstract

“…The disease has a variable clinical course, progression and survival rate. It is proposed that CLL cell growth, survival and expansion are driven by unknown antigens/autoantigens through the B-cell antigen receptor (BCR), and supported by microenvironmental signals (3) including the toll-like receptors (TLRs), in particular CD180/RP105 (4,5) and TLR9 (6)(7)(8)(9)(10). CD180/RP105 is a membrane-associated orphan receptor that drives normal human and mouse B-cell activation and proliferation (11)(12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

Rewiring of sIgM-Mediated Intracellular Signaling through the CD180 Toll-like Receptor

Porakishvili

Vispute

Steele

et al. 2015

Mol Med

View full text Add to dashboard Cite

Chronic lymphocytic leukemia (CLL) development and progression are thought to be driven by unknown antigens/autoantigens through the B cell receptor (BCR) and environmental signals for survival and expansion including toll-like receptor (TLR) ligands. CD180/RP105, a membrane-associated orphan receptor of the TLR family, induces normal B cell activation and proliferation and is expressed by approximately 60% of CLL samples. Half of these respond to ligation with anti-CD180 antibody by increased activation/phosphorylation of protein kinases associated with BCR signaling. Hence CLL cells expressing both CD180 and the BCR could receive signals via both receptors. Here we investigated cross-talk between BCR and CD180-mediated signaling on CLL cell survival and apoptosis. Our data indicate that ligation of CD180 on responsive CLL cells leads to activation of either prosurvival Bruton tyrosine kinase (BTK)/phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/AKT-mediated, or proapoptotic p38 mitogenactivated protein kinase (p38MAPK)-mediated signaling pathways, while selective immunoglobulin M (sIgM) ligation predominantly engages the BTK/PI3K/AKT pathway. Furthermore, pretreatment of CLL cells with anti-CD180 redirects IgM-mediated signaling from the prosurvival BTK/PI3K/AKT toward the proapoptotic p38MAPK pathway. Thus preengaging CD180 could prevent further prosurvival signaling mediated via the BCR and, instead, induce CLL cell apoptosis, opening the door to therapeutic profiling and new strategies for the treatment of a substantial cohort of CLL patients.

show abstract

Toll-Like Receptors in Chronic Lymphocytic Leukemia

Cited by 22 publications

References 94 publications

Extracellular vesicles released from chronic lymphocytic leukemia cells exhibit a disease relevant mRNA signature and transfer mRNA to bystander cells

Extracellular vesicles released from chronic lymphocytic leukemia cells exhibit a disease relevant mRNA signature and transfer mRNA to bystander cells

Quantitative Expression of Toll-Like Receptors TLR-7 and TLR-9 on Peripheral Blood Mononuclear Cells in Leukemias

Rewiring of sIgM-Mediated Intracellular Signaling through the CD180 Toll-like Receptor

Contact Info

Product

Resources

About