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Table 1 miRNAs and B cell functions

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]

  1. TB, tuberculosis; CTRL, control; BL, Diagnosis; M1, month 1; M6, month 6; GC, germinal center; SLE, systemic lupus erythematosus; DLBC, diffuse large B-cell lymphoma; RA, rheumatoid arthritis; ERA, early rheumatoid arthritis; LSRA, long standing rheumatoid arthritis; BCR, B cell receptor; CLP, common myeloid progenitor; LA, lactic acid; MLL, myeloid/lymphoid leukemia; ALL, acute lymphoblastic leukemia; BL, Burkitt lymphoma; SLE; systemic lupus erythematosus; PTLD, posttransplant lymphoproliferative disorder; EBV; Epstein-Barr virus; BCL, B-cell lymphoma; cGVHD, Chronic graft-versus-host disease; BO, bronchiolitis obliterans; B NHL, B cell non-Hodgkin’s lymphoma; OS, overall survival; EFS, event free survival; WT, wild-type; KO, knockout; TG, overexpression; IM, Imatinib; CML, Chronic myeloid leukemia; PCNSL, Primary lymphomas of the central nervous system; SCNSL, secondary spread of systemic lymphoma to the CNS; CSF, Cerebrospinal fluid; ECOG, Eastern Cooperative Oncology Group; IPI, International Prognostic Index; B-ALL, B-cell acute lymphoblastic leukaemia; DFS, disease-free survival; PBC, Primary biliary cholangitis; ANCTs, adjacent non-cancerous tissues; BMT, bone marrow transplantation; ABMR, Antibody-mediated renal allograft rejection; PMBL, Primary mediastinal large B-cell lymphoma; LNRH, lymph node reactive hyperplasia; RPL, reactive proliferative lymphadenitis; PBMCs, Human peripheral blood mononuclear cells; DS, Down Syndrome; DM, diabetes mellitus; RLH, reactive lymph node hyperplasia; AML, acute myeloid leukemia; ITP, immune thrombocytopenia; KD, Kawasaki disease; IgAN, immunoglobulin A nephropathy; RLH, reactive lymphoid hyperplasia; LRH, lymphonode reactive hyperplasia; cHL, Classical Hodgkin lymphoma