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. 2020 Dec 9;10:604685. doi: 10.3389/fonc.2020.604685

Table 3.

B cell lymphoma and B-cell receptor (BCR) antigens.

B-cell neoplasia Expression of sIg Indications for chronic BCR stimulation by an antigen or alternative BCR pathway activation
CLL Yes, dim

  • subsets with stereotypic CDR3 (181)

  • specific autoantigens for individual subsets (129, 134, 176, 182)

  • specific microbial antigens (139)

  • concept of autonomous, antigen-independent BCR signaling mediated by anti-framework region reactivity (142)

  • clinical effectivity of BCR pathway inhibition (133)
MCL Yes

  • subgroup with stereotypic CDR3s (152)

  • subgroup with BCR-reactivity and autoantibodies against LRPAP1 (183)

  • reactivity against protein A of Staphylococcus aureus (184)

  • clinical effectivity of BCR pathway inhibition (156, 159)
FL Yes

  • gains of N-glycosylation sites in BCR yield in binding to lectins (126)

  • pediatric FL: cervical manifestation, speculation about infectious trigger

  • duodenal FL: speculations about infectious trigger
HCL Yes

  • classic HCL hints for affinity maturation (145, 185)

  • variant HCL regularly IGHV4-34

MZL Yes

  • splenic MZL: strong association with HCV (100, 101)

  • MALT-lymphoma of the stomach: strong association with H. pylori (94, 95)

  • MALT-lymphoma of ocular adnexes: reported association with Chlamydia psittaci (99)

  • MALT-lymphoma of salivary glands after Sjögren’s syndrome: autoreactive BCR (125)

  • effectivity of BCR-pathway inhibition (186)
cHL No

  • destructive IgV gene mutations in 25% of cases (187, 188)

  • *ITAM-signal of EBV-encoded LMP2a mimicking activated BCR (117)
NLPHL Yes

  • reported predominance of Igκ-light chains (189)

  • IgD+ subgroup with cervical manifestation (190)

  • Moraxella catarrhalis RpoC as antigen of IgD+ LP-cells with extraordinary long CDR3s (107)

  • However, clinical trials with BTK-inhibition in r/r NLPHL failed
BL Yes

  • concept of tonic BCR activation by mutation in ID3 and TCF3 ( 83)

  • suspected stimulation by Plasmodium falciparum of EBV-infected centroblasts in endemic BL (111, 112)

  • reports of modified autoantigens in sporadic BL (191)
DLBCL in subgroups
Yes		 ABC-type

  • activating mutations in CD79B und MYD88 (66, 87) of MCD type, cluster 5 or ABC-type

  • reported autoreactivity of OCI-Ly10, U2932 lines (169), reactivity against FR2 of TDM8 line, cis and trans stimulation by an autoantigen for HBL1, reactivity of CDR3 of TDM8 against FR2 (V (37)R (38)) of TDM8 (169)

  • ARS2 identified as frequent target antigen of ABC-type DLBCL. ARS2 hypophosphorylated in these cases.

  • effectivity of BCR-pathway inhibitors (192, 193)


PCNSL

  • overrepresentation of auto-reactivity associated IGHV4-34 ( 194)

  • activating mutations in CD79B und MYD88 ( 195)

  • reported poly-reactivity of BCR (196)

  • SAMD14/neurabin-I identified as target of BCRs SAMD14/neurabin-I hyper-N-glycosylated in these patients (173)

  • effectivity of BCR-pathway inhibitors (197, 197)

  • PIOL shares biologic characteristics with and frequently progresses to PCNSL and shares overrepresentation of IGHV4-34 (198)


PTL

  • frequently shares activating mutations in CD79B und MYD88, with other aggressive lymphomas of immunologically privileged sites
PMBCL No

  • probably independent of BCR (199)
LPL Yes

  • clinical effectivity of BCR pathway inhibition (200, 201)

  • post-translationally modified SLP2 and HSP90 as specific antigens (paratargets) of IgM paraproteins (171, 175, 180)
MM only secreting, no sIg

  • posttranslationally modified SLP2, HSP90, sapC as specific antigens (paratargets) of paraproteins (171, 175, 180)