From: The emerging role non-coding RNAs in B cell-related disorders
microRNA | Expression pattern | Disease/ | Sample | Cell line | Interaction | Signaling pathway | Function | References |
---|---|---|---|---|---|---|---|---|
Human studies | ||||||||
miR-16–1 | ↓ | DLBC | 40 untreated patients diagnosed with DLBC and 15 healthy controls | CD19( +) and CD20( +) cells | – | – | – | [11] |
miR-15a | no difference | DLBC | 40 untreated patients diagnosed with DLBC and 15 healthy controls | CD19( +) and CD20( +) cells | – | – | – | |
miR-150 | ↑ (lower in GC B cell than the other two subsets) | chronic tonsillitis | children with chronic tonsillitis | Naïve B cells, GC B cells and memory B cells | c-Myb, Survivin and Foxp1 | – | ↑ miR-150: ↑ the amount of apoptotic/death cells, ↓ c-Myb, Survivin and Foxp1 | [10] |
miR-155 | ↑ (abundantly in synovial B cells) | RA | 27 patients with ERA and 33 patients with LSRA, 14 patients with osteoarthritis, 9 healthy controls | B cells, CD19 + cells, synovial B cells | PU.1 | – | ↑ RA B-cell activation associated with autoantibody production ∆ miR-155: ↓ antibody synthesis | [15] |
viral miR-BHRF1 | ↓ | EBV-immortalized B lymphoblastic cell malignancy | – | Ramos and BJAB, Manassas, VA, B95.8, HEK293 | SMAD3, JUN, and COL1A | TGF-β signaling pathway | LA: ↓ viral miR-BHRF1-1: ↑ adhesion and the growth of EBV-infected B cells | [18] |
miR-28 | ↓ | BL | – | GC B cells, HEK293T cells and B-cell lines | MAD2L1, BAG1, MYC | – | ↓ proliferation and clonogenic properties of BL cells, MYC-induced transformation | [19] |
miR-19a | ↑ | sepsis | 64 patients with SIRS and 15 healthy controls | PBMCs | CD22 | BCR signaling | ↑ BCR signaling | [13] |
miR-30a | ↑ | SLE | patients with SLE and healthy controls | Daudi and Raji B cell lines | Lyn | – | ↑ B cell proliferation and the production of IgG antibodies through inhibiting Lyn | [14] |
miR-194 | ↓ | PTLD | PBMC or lymph node from six PTLD patients and 4 healthy blood donors | AB5, JB7, JC62, MF4, VB5, ZD3 derived from PBMC or lymph node of six PTLD patients and B lymphoblastoid cell lines isolated from 4 healthy blood donors | IL-10 | – | Expression of microRNA-194 was suppressed by EBV microRNA-194 inhibited IL-10 expression, so reduced proliferation and promoted apoptosis of EBV( +) B cell lymphoma lines | [20] |
miR-125b | ↑ | – | – | murine Bcl1.3B3 B lymphoma and the human U266 multiple myeloma cell lines | BLIMP-1 and IRF-4 | – | ↓ differentiation of GC centroblasts and myeloma cell survival through inhibiting BLIMP-1 and IRF-4 translation | [21] |
miR-148b | ↓ | BCL | Peripheral blood from 21 patients with BCL and 18 healthy controls, Lymphatic tissue from 30 patients with BCL and 20 healthy controls, male BALB/c nude mice | Raji and SU-DHL-10 human BCL cell lines, HEK-293 T | Bcl-w | – | ↓ cell viability, colony formation, and ↑ apoptosis in irradiated BCL cells, ↓ growth of tumors in nude mice (↑ radiosensitivity of BCL cells) | [22] |
miR-197 | ↓ | DLBCL | 51 patients with DLBCL | SUDHL9 and OCI-LY1 human DLBCL cell lines | – | – | ↑ miR-197: ↑ effects of doxorubicin on reducing cell viability and enhancing apoptosis | [12] |
miR-124 | ↓ | DLBCL | – | OCI-Ly1 and HBL1 | p65 | TAK1/IKKα-IKKβ/IκBα and MAPK/p65 signaling pathways, NF-κB signals | ↓ cell proliferation and survival | [23] |
miR-17–92 | ↑ | B-NHL | 71 patients with B-NHL, 5 patients with reactive hyperplasia lymph nodes as controls, female Balb/c nude mice | WT, KO and TG lymphoma cells and reactive hyperplasia lymph cells obtained from mice | – | – | ↑ miR-18: ↓ OS ↑ miR-19 and miR-92a: ↓ OS and EFS ↑ miR-17–92: ↓ the duration of incubation required for visualization of the xenograft tumor | [24] |
miR-155 | – | DLBCL | 76 patients with DLBCL | HEK293T, RIVA, U2932, DHL4, HBL-1, Ly7, Ly18, and Ly19 cell lines | DEPTOR and c-CBL | BCR signaling | ∆ mir-155: ↓ expression of NFkB target genes and ↑ sensitivity DLBCL cells to ibrutinib Low expression of DEPTOR (a target of mir-155) increased the migration of DLBCL cells toward the CXCL12 gradient and modulated cytokine production | [25] |
miR-320d | ↓ | DLBCL | 85 patients with DLBCL, 19 samples with lymph node reactive hyperplasia as controls | OCI-LY1 (GCB subtype) and NU-DUL-1 (ABC subtype) human DLBCL cell lines | CDK6 | – | ↓ proliferation in GCB type of DLBCL cells and ↓ CDK6 expression | [26] |
miR-195 | ↓ | DLBCL | 60 patients with DLBCL and 30 healthy controls | – | – | Expression levels of miR-195 closely correlated with tumor diameter, IPI score and Ann Arbor stage Patients with high levels of miR-195 had longer OS | [27] | |
miR-155 | ↓ in vincristine- resistant DLBCL cell lines | DLBCL | 73 patients with DLBCL, GEO database: data (GSE10846 and GSE31312) | U-DHL-5 and OCI-Ly7 GCB-DLBCL cell lines, RIVA and NU-DHL-1 ABC cell lines | Wee1 (a direct target of miR-155) | – | ↑ sensitivity to vincristine Expression level of miR-155 was strongly correlated with superior survival for R-CHOP-treated patients of the GCB subclass | [28] |
miR-153-3p | ↓ in IM-resistant CML cells | CML | Blood samples obtained from 44 CML patients | human KBM5, K562 and IM-resistant KBM5R, K562R CML cell lines | Bcl-2 (a direct target of miR-153-3p) | – | ↑ miR-153-3p: ↑ IM sensitivity and ↓ the survival rate of IM-resistant CML cells ↓ autophagy caused by IM in IM-resistant CML cells | [29] |
miR-30c | ↑ in patients with SCNSL | PCNSL, SCNSL | 61 CSF samples from patients with PCNSL and 14 samples from SCNSL | – | – | – | miR-30c could act as a biomarker to distinct PCNSL from SCNSL | [30] |
miR-155 | ↑ | NHL and DLBCL | 84 patients with B-cell NHL and 15 healthy controls | – | – | – | Higher levels of miR-155 were correlated with the presence of B symptoms, involvement of extranodal sites, and high ECOG score In DLBCL, higher levels of miR-155 were correlated with non-germinal B-cell-like type, the presence of B symptoms, involvement of extranodal sites, and higher IPI and ECOG scores ↑ miR-155; ↑ lower event-free survival | [16] |
hsa-miR-34a-5p | ↑ | DLBCL | six serum samples from patients with DLBCL and 3 healthy control | – | TP53 | p53 signaling pathway | hsa-miR-34a-5p was involved in 15 pathways such as the p53 signaling pathway | [31] |
hsa-miR-323b-3p | ↓ | DLBCL | six serum samples from patients with DLBCL and 3 healthy control | – | – | – | hsa-miR-323b-3p was involved in four pathways such as pathways in cancer | |
hsa-miR-431-5p | ↓ | DLBCL | six serum samples from patients with DLBCL and 3 healthy control | – | FYN | – | regulating FYN | |
miR-155 | ↑ in EBV-infected B cells | lymphoma | – | DG75 cell line originated from an EBV-negative BL, DG75 RBPJ knockout cell line derived from DG75 wt parental cells, IB4 and GM12878 obtained from Coriell Cell Repositories (EBV-immortalized lymphoblastoid cell lines) | EBNA2, IRF4, RBPJ | – | ↑ the growth of EBV-infected B cells | [32] |
miR-3173 | ↓ | B-ALL | GEO database (GSE4732, GSE4475, GSM565540) 135 children with B-ALL and 97 healthy controls plus 430 children with B-ALL and 340 healthy controls | CCRF-SB and SUP-B15 human B-ALL cell lines | PTK2 (a direct target of miR-3173) | – | ↓ proliferation, migration and invasion | [33] |
miR-21 | ↑ | B-ALL | 75 children with B-ALL and 50 healthy controls | – | – | – | Lower DFS and OS | [34] |
miR-21 | ↑ | DLBCL | 36 tissue samples from 26 patients with DLBCL and 10 healthy controls | CRL-2630 | PTEN | – | higher in stage III/IV patients, ↓ apoptosis (by regulating the expression of PTEN) | [35] |
miR-222-3p | ↑ | DLBCL | 74 patients with initial diagnosis of ABC-type DLBCL, 26 patients with pathological diagnosis of reactive lymphoid hyperplasia as controls, SPF BALB/c nude mice | HMy2.CIR human normal B-cell immortalized cell line, DLBCL cell line, germinal central B-cell (GCB)-like OCI-Ly19 and SU-DHL-4, and ABC-like OCI-LY10 and U2932 | Phosphatase 2 regulatory subunit B alpha (a direct target of miR-222-3p) | – | ↑ proliferation, invasion and tumor growth, ↓ apoptosis | [36] |
miR-29a | ↓ | SLE | peripheral blood of 66 patients with SLE and 10 healthy controls | Raji, | CRKL (a target gene of miR-29a) | – | ↓ the production of IgG (by regulating CRKL) | [37] |
hsa-miR-223-3p and hsa-miR-21-5p | ↓ from stage I to stage III of PBC | PBC | Peripheral B cells from 72 PBC patients and 15 healthy controls | – | mutual 4 target genes: TGFBR2, MEF2C, FOXP1 and RBPJ | – | modulating B cell functions, such as B-cell signal transduction, differentiation, migration, and apoptosis in GO categories | [38] |
miR33b, miR96, and miR503 | ↓ | Lymphoma | – | JeKo-1, Pfeiffer, SUDHL-2, PDX, and A20 | PRMT5, CYCLIN D1 and c-MYC (target genes of miR33b, miR96 and miR503) | – | ↓ lymphoma cell survival | [39] |
miR-214 | ↓ | DLBCL | 15 pairs of DLBCL tissues and ANCTs, female BALB/c nude mice | OCI-Ly3, SU-DHL-2 and OCI-Ly10 human DLBCL cell lines, a normal B-cell line (NBC) and HEK-293 T | PD-L1 | – | ↓ viability and invasion, ↑ apoptosis | [40] |
miR-107 | ↓ | ABMR | 19 patients with ABMR and 20 healthy controls | B lymphocytes, Daudi, Raji, and HEK-293 | ATG12 | – | ↑ miR-107: ↓ formation of autolysosomes in B lymphocytes of recipients, autophagy, and secretion of IgG and IgM antibodies | [41] |
miR-92a | ↑ in PMBL than in DLBCL, but not in cHL | PMBL, DLBCL, cHL | 40 patients with PMBL, 20 patients with DLBCL, and 20 patients had with cHL | Karpas-1106P, SU-DHL-5 | FOXP1 (a target of miR-92a) | – | ↓ proliferation, ↑ apoptosis, | [42] |
miR-21 | ↑ | DLBCL | 45 samples of lymphoma tissues from patients with DLBCL | SU-DHL-8, OCI-LY1, and SU-DHL-10 | VHL (a target of miR-21) | – | Curcumin decreased the proliferation, migration, and invasion abilities and increased apoptosis by suppressing miR-21 | [43] |
miR-155 | ↑ | DLBCL | 76 patients with DLBCL and 40 samples with | DB cells | – | – | ↑ migration and invasion, ↓ apoptosis | [44] |
miR-215 | ↓ | DLBCL | 50 patients with DLBCL and 30 samples with RPL | SU-DHL-4 cells | KDM1B | – | ↓ proliferation and ↑ apoptosis Low levels of miR-215 were correlated with shorter 5-year OS | [45] |
miR-155 | ↑ in tonsillar memory B cells and PBMCs activated with CpG | DS | – | PBMCs and Tonsils from healthy controls and children with DS | AID (a target of miR-155) | – | miR-155 played a role in DS-associated dementia and leukemia | [46] |
miR-125b | ↑ in tonsillar memory B cells and plasma cells | DS | – | PBMCs and Tonsils from healthy controls and children with DS | – | – | miR-125b played a role in DS-associated dementia and leukemia | |
miR-98 | ↑ | asthma | 20 patients with asthma and 20 healthy controls | PBMCs from healthy controls and patients with asthma | TSP1 | – | IL-13 decreased TSP1 expression through up-regulating expression of miR-98 in B cells | [47] |
miR-28-5p | ↓ | DLBCL | – | OCI-LY7 human GCB-type DLBCL cell line and HEK-293 T | BECN1 (a direct target of miR-28-5p) | – | Curcumin: ↑ miR-28-5p: ↓ proliferation and autophagy, ↑ apoptosis | [48] |
miR-21 | ↑ | DLBCL | 53 patients with DLBCL | – | Ki-67 | – | High expression levels of miR-21 was correlated with poor response to treatment | [49] |
miR-10a | ↓ | DLBCLs | 9 patients with DLBCL and 9 samples with RLH as controls | OCI-LY7 and OCI-LY3 human DLBCL cell lines and HEK293T | BCL6 (a direct target of miR-10a) | – | ↓ proliferation, ↑ apoptosis | [50] |
miR-125a | ↓ | AML | – | HL60 | p53, Bcl-2, c-myc | NF-κ Pathway | ↑ miR-125a: ↓ viability and invasion, ↑ apoptosis | [51] |
let-7b-5p | ↑ | ITP | 61 patients with ITP and 31 healthy controls | PBMC from samples, peripheral CD19 + cells | BAFF, BAFF-R, NF-κB2 p100, Bcl-xL | – | ↑ B cell survival, ↑ BAFF-R and BAFF levels, ↑ phosphorylation of NF-κB2 p100 | [52] |
miR-27a | ↑ | KD | 23 children with acute KD and 23 healthy controls | PBMCs from samples, PurifiedCD19 + B cells, CD14 + monocyte cells | IL-10 | – | ↑ monocyte-mediated TNF-α release, ↑ monocyte-mediated inflammatory responses via inhibiting the regulatory function of B10 cells | [53] |
miR-17–92 | – | – | C57BL/6 mice | 38c13 cells, HEK, CD19KO B cells | c-Myc, PTEN (a target of miR-17–92) | PI3K/Akt/Foxo1 pathway | ∆ miR-17–92: ↑ RAGs expression (post-translationally through Foxo1) miR-17–92: ↓ B cell development | [54] |
miR-4638-5p | ↓ in ERG + DLBCL | DLBCL | 126 patients with DLBCL (in Kaplain‐Meier survival analysis) and 94 patients with DLBCL (in the clinicopathologic correlation study) | – | ERG | – | More mutations in genes important in cell cycle control, B-cell receptor-mediated signaling and degradation of β-catenin were seen in ERG + DLBCL more likely harbors | [55] |
miR-518a-5p | ↓ | DLBCL | 56 samples with DLBCL and 29 samples with RLH as controls | HMy2.CIR normal B cell line, SU-DHL-2 and SU-DHL-6 DLBCL cell lines | CCR6, (a direct target of miR-518a-5p) | JAK2-STAT6 signalling pathway | There is a negative regulatory feedback loop between miR-518a-5p and CCR6 in DLBCL ↑ miR-518a-5p: ↓ proliferation and invasion, ↑ apoptosis | [56] |
miR-296-5p | ↑ | DLBCL | – | DLBCL-DB cells | – | – | ∆ miRNA-296-5p: ↓ proliferation and migration, apoptosis did not change | [57] |
miR-34a | ↓ | DLBCL | 65 patients with DLBCL and 22 samples with LRH as controls | – | ↑ BCL-2 | – | Patients with high levels of miR-34a had longer OS | [58] |
miR-224 | ↓ | DLBCL | 76 patients with DLBCL and 41 healthy controls | – | PIK3CD (a direct target of miR-224) | – | ↑ miR-224: ↓ proliferation and invasion, ↑ apoptosis | [59] |
miR-451a | ↓ | DLBCL | 89 patients with DLBCL and 48 healthy controls | – | – | – | The efficacy of rituximab combined with chemotherapy can be evaluated by miR-451a as an indicator | [60] |
miR-152-3p | ↑ | SLE | 30 female patients with active SLE and 30 female healthy controls | SLE B-cells | KLF5 (a direct target of miR-451a), BAFF | – | ∆ miR-152-3p: ↓ self-reactivity of SLE B-cells, and ↓ autoantibody production | [61] |
miR-28 | ↓ in GC-derived neoplasms | Non-Hodgkin lymphoma | human primary GC-derived B-cell neoplasms (GSE 29,493), NSG mice | naïve B cells (CD19 + GL7 −), GC B cells (CD19 + GL7 +), and post-GC B cells (CD19 + GL7 − IgA +) from Peyer’s patches Ramos and Raji BL GC-derived B-cell lines and MD901 DLBCL cell line | – | BCR signaling | Downregulation of miR-28 expression is correlated with GC B-cell transformation ↑ miR-28: ↓ proliferation and survival | [62] |
miR-98 | ↑ | heart transplantation | peripheral blood samples from 20 patients with advanced heart failure before and after and 20 healthy controls, male BALB/c mice and male C57/B6 mice | peripheral blood mononuclear cells were isolated from the blood samples | ↓ IL-10 | – | The levels of miR-98 and serum levels of cortisol were increased in peripheral B cells after heart transplantation Cortisol-suppressed IL-10 expression was mediated by miR-98 | [63] |
miR-21-5p | ↑ in cHL than GC-B cells | cHL | – | L540, KM-H2, L1236, L428 and L591, SUPHD1 CHL cell lines and HEK-293 T | PELI1 | – | ∆ miR-21-5p: ↓ growth, ↑ apoptosis | [64] |
miR-29a | ↓ | Arthritis | – | miR-29a knockout mice | – | – | ↑ B-cell activation and germinal center production | [65] |
miR-126 | ↓ in MLL-AF4 ALL | ALL | Congenic mice | Ebf1 − / − hematopoietic progenitor (Lin −) cells were isolated from the Ebf1 − / − livers of 14 d postcoitum embryos | IRS-1 | – | miR-126 drived B-cell myeloid biphenotypic leukemia differentiation toward B cells. (↑B cells) miR-126 could partly rescue failed B-cell lineage development and specification | [66] |
miR-212 | ↑ | Autoimmune disease and cancer | C57BL/6 WT and miR-212/132 − / − mice | HEK293T, primary splenic B cells | – | BCR signaling | BCR activation: ↑ miR-212 | [67] |
miR-132 | ↑ | Autoimmune disease and cancer | C57BL/6 WT and miR-212/132 − / − mice | HEK293T, primary splenic B cells | Sox4 | BCR signaling | BCR activation: ↑ miR-132 ↓ early B cell development, ↑ apoptosis in primary bone marrow B cells ∆ miR-132: B cell recovery after antibody-mediated B cell depletion ↓ B cell leukemia development | |
mir-23a cluster | – | – | mirn23a − / − mice and WT C57BL/6 mice | A20 and EML, 32Dcl3 | Ebf1, Pax5, Mef2c, Ikzf1, FoxO1, Trib3 | – | ∆ mirn23a: ↑ B cells, ↑ B lymphopoiesis, ↑ T1 population of transitional B cells, ↑ CLP population and ↓ myeloid cells, ↓ myelopoiesis, ↓ myeloid progenitor populations B cells with mirn23a − / − genotype secrete normal levels of IgG, proliferate normally, and could differentiate into short-lived effector plasma cells in response to antigen | [68] |
miR-148a | ↑ | Lupus | gMb-macroself, Gadd45a − / − , Bcl2l11 − / − , Ptenfl/fl, Cd19-Cre, Tnfrsf1b − / − mice, and CD45.1 + C57BL/6 J mice | HEK293T, splenic B cells (CD19 +) and BM B cell precursors (CD19 + IgM −) from CD45.1 + C57BL/6 J mice | Gadd45α, PTEN, Bim | – | miR-148a was found to be a regulator of B cell tolerance by promoting the survival of immature B cells and accelerating the development of autoimmunity by suppressing the expression of Gadd45α, PTEN, Bim | [69] |
miR-17–92 | ↑ | cGVHD | miR-17–92 conditional knockout mice (BALB/c mice) | donor BM-derived cells (Ly5.1 +) in peripheral blood and spleen, miR-17–92–deficient B cells, | – | – | miR-17–92 increases the pathogenicity of B cells, promoted GC responses and B-cell function, the development of BO and reduced proteinuria/ascites | [70] |
miR-125b | Epigenetic silencing of miR-125b is necessary for normal B-cell development | – | WT and Eμ/miR-125b-Tg mice | HEK293T, bone marrow sinusoidal and parenchymal B cells from Eμ/miR-125b-Tg mice and littermate controls | S1PR1, IRF4 | – | Expression of miR-125b impaired B-cell egress from the bone marrow to peripheral blood | [71] |
miR-26a | ↓ in DLBCL cell lines compared to B lymphocytes | DLBCL | NOD/SCID mice | SU-DHL-4, SU-DHL-6, SU-DHL-16 GCB cell lines and SU-DHL-2, SU-DHL-8, and RCK-8 ABC cell lines | CDK5, p35 (a direct target of miR-26a) | – | ↓ DLBCL tumor growth, proliferation, cell-cycle progression, and survival | [72] |
miR-155 | – | – | CD45.1 + congenic mice, SWHEL mice and miR-155–deficient mice (all with the C57BL/6 background) | SWHEL Mir155 + / + or SWHEL Mir155 − / − donor B cells | – | – | miR-155 regulated the early expansion of B-blasts and later on the survival and proliferation of plasmablasts in a B-cell-intrinsic manner miR-155 is required for the optimal proliferation of plasmablast B cells | [73] |
miR-181b | ↑ in neonatal B cells | – | miR-181a/b1−/− mice; ko mice and miR-181a/b-1 ± mice with C57BL/6 J background | Neonatal and adult B cells | – | – | ∆ miR-181b: ↑ class-switch recombination | [74] |
miR-155 | ↓ | chronic psychological stress | male C57BL/6 mice | In-vitro-induced GC B cells, Naive B cells, Su-DHL4 cells | FBXO11 (a direct target of miR-155), BCL6 | – | Corticosterone treatment: ↓ miR-155: ↓ GC B cell generation and isotope class switching ↑ miR-155: ↓ stress-induced impairment of GC response | [17] |
miR-221 | – | – | C57BL/6, RAG1−/−(CD45.2, CD45.1) mice | preBI cell lines | PTEN (a target of miR221), CXCL12, Bcl2 | PI3K signaling | ↑ precursor B-cell retention in the bone marrow, ↑ CXCR4-PI3K mediated Bcl2 upregulation, ↑ early B-cell adhesion capability via PI3K signaling | [75] |
miR-92a | ↓ | DM | Adult mice | Min-6 mouse pancreatic bcells | KLF2 (a direct target of miR-92a) | – | ↑ insulin secretion and proliferation, ↓ apoptosis | [76] |
miR-15a/16–1 | ↓ | Plasma cell and mature B-cell neoplasms | AIDCre/ + (wild-type [WT]) control and AIDCre/ + ;miR-15a/16-1 fl/fl (knockout [KO]) compound mice with C57BL/6 background | GC B cells from WT and KO mice | – | – | Deletion of the miR-15a/16–1 increased the number of GC B cells, percentage of dark zone B cells, and maturation into plasma cells | [77] |
miR-146a | – | – | CD21-cre, Cγ1-cre, CD4-cre, hCD2-cre, and CD40-deficient mice, B-KO/CD40 + / − mice | Naive B cells from unimmunized B-KO mice or WT littermates and GC B cells from corresponding D14 SRBC-immunized mice | – | CD40 signaling pathway | The loss of miR-146a in B cells leaded to the development of spontaneous autoimmunity miR-146a is crucial to maintain optimal B cell responses | [78] |
miR-146a | ↓ | B-cell oncogenesis | Eμ-Myc miR-146a − / − mice | 70Z/3 and WEHI-231 | Egr1, Blimp1 and Bcl6 | – | ↓ miR-146a: ↓ survival, ↑ in peripheral blood CD11b + myeloid cells, ↑ mature B-cell phenotype ↑ miR-146a: ↓ cell growth | [79] |
miR-21 | ↑ | Lymphoma | NOD-SCID mice | OCI-LY3 and Ramos, OCI-LY10, U2932, Raji, Rec-1, Jeko-1, Maver-1 and JM1, HEK293T | Nl101, Mxd1 (a target of miR-21), c-Myc | – | NL101: ↑ miR-21, c-Myc: ↓ miR-21, miR-21: ↑ proliferation and survival, ↓ apoptosis | [80] |
miR-146a | ↓ | Immune complex glomerulonephritis | miR-146a − / − mice with C57BL/6 background | B lymphocytes were the spleen, HK-2 | Kim1/Tim1 | – | ∆ miR-146a: ↑ numbers of memory B cells and plasmablasts, ↑ glomerular hypercellularity with age , ↓ Bregs and ↓ Kim1/Tim1 | [81] |
miR-146a | ↑ | – | Murine OVA-Induced asthma mice, WT and miR-146a TG mice | purified splenic B cells | Smad4 (a direct target of miR-26a), 14–3-3σ | – | ↑ class switch and secretion of IgE in B cells | [82] |
miR-142 | ↑ | Lymphoma | BMT and transgenic (Eμ/mir142) mice | KHM10B, Raji, KMS12, OCI-Ly8, Hut 78, and Cos7 | – | – | In splenic B cells, high expression of Mir142 modified LPS-induced phenotypical changes | [83] |
miR-7 | ↑ | SLE | Female MRLlpr/lpr lupus mice | Purified splenic B cells obtained from mice | PTEN | PTEN/AKT signaling | ∆ miR-7: ↓ nephritis, ↓ lupus manifestations, ↓ immune Abnormalities, ↓ tfh-derived IL-21 expression, ↓ Abnormal B cell differentiation, normalizes splenic B cell subtypes | [9] |
miR-98 | ↑ | Myocarditis | BALB/c mice immunized with MyHC-α | B cells isolated from the mouse hearts with myocarditis | ↓ IL-10 (a target of miR-98), TNF-α | – | ∆ miR-98: ↓ myocarditis miR-98 is upregulated by TNF-α in B cells | [84] |
Let-7 | – | – | Lin28a iTg mice, let-7adf cluster KO mice, and let-7bc cluster KO mice | HEK293T | Hk2 (a target gene of Let-7) c-myc (a target gene of Let-7) Slc1a5 and Gls (indirect target genes of Let-7) | – | ↓ IgM Production ↓ glycolytic capacity and glucose uptake ↓ glutamine uptake and utilization ↓ B Cell Activation | [85] |
Let-7 | ↑ in thymic B progenitors by in vitro co-culture with IL15, Vitamin-D3, and retinoic acid | – | Foxn1lacZ/lacZ (Z/Z) mice with C57Bl6/J background, Foxn1nude heterozygous (Foxn1 + /nude) mice with C57Bl6/J background, Foxn1lacZ/nude (Z/N) mice, Foxn1 + /lacZ (+ /Z) mice | thymic progenitor B cells | Lin28a, Arid3a | – | ↓ B cell production in the thymus, ↓ proliferation of intrathymic progenitor B cells | [86] |
miR-191 | ↑ during B-cell development and differentiation | – | C57BL/6 J and NOD.Cg-PrkdcscidIl2rgtm1Wjl/SzJ (NSG) mice, C57BL/6 mice and miR-191 − / − mice | Primary cells from wild-type or chimeric mice, preB1 cells, | Foxp1, E2A, and Egr1 | – | Expression levels of miR-191 are required for efficient B-cell development, V(D)J recombination and IL-7-dependent expansion of preBI cells | [87] |
miR-15 family | ↓ | – | Female C57BL/6 Rag1 − / − mice | wk3, 1587, and 1677 pre‐B cell lines from total bone marrow of SLP‐65 − / − and SLP‐65 − / − LAT − / − mice, respectively, and 1676 and 74 pre‐B cell lines | ↑ cyclin E1 and D3 | – | The lack of miR-15 family in pre-B cells caused prolonged proliferation, so failed to trigger the transcriptional reprogramming to accompany their differentiation | [88] |
mirn23a cluster | ↓ | – | Wildtype and mirn23a−/− C57BL/6 mice, CD45.1 recipient mice, femurs and tibias of mice | 70Z/3, A20 and 32Dcl3 cell lines | ↑ Ikzf1, Runx1, Satb1, Bach1 and Bach2 that managed the commitment of MPPs to CLPs ↑ FoxO1, Ebf1, and Pax5 that commited the CLP to the B cell lineage in the absence of mirn23a, EBF1 | PI3K/Akt and BMP/Smad signaling pathways | Mirn23a regulated some related transcription factors and signaling pathways to modulate adult hematopoiesis Mirn23a was inhibited by EBF1 | [89] |