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PubMed1993

Replacement of HLA class II serology by the HLA-DR microtitre plate oligotyping assay: a one-year experience in unrelated bone marrow donor selection.

Because the selection of unrelated bone marrow donors requires a more accurate HLA-typing technique than is used for sibling donors, we have replaced class II serology by a rapid and highly discriminative HLA-DR DNA oligotyping assay on microtitre plates. We present here our 1-year experience with class II typing for 112 potential donors identified for 33 consecutive leukaemic patients. Although the donors were selected to be HLA-A, -B, -DR serologically identical, the microtitre plate oligotyping assay detected DR incompatibilities in 52.7% of the patient/donor pairs. One third was due to incorrect or incomplete typing of DR11 to DR16, the others to mismatches for the serologically indistinguishable subtypes of DR1, 11, 13 and 15, known to be relevant for T cell recognition.

Bone Marrow Transplantation↗
PubMed1993

[DNA typing of the three HLA-class II loci from saliva stains].

The DNA typing of the HLA-class II loci, HLA-DPB1, HLA-DQA1 and HLA-DRB, from saliva stains is described. In addition to the experimentally prepared saliva stains, a stain on a towel in a burglar case was subjected to the analysis. Using 10 ng of the extracted DNA, we could type all the three loci with all of the specimens tested. The incidence of the saliva stain in the practical case was estimated to be 3.18 x 10(-5) in Japanese population. We found that the aging of saliva stains at least six months did not significantly influence the DNA typing.

DNA↗
PubMed1987

Anti-HLA-class II monoclonal antibodies inhibit polyclonal B cell differentiation in vitro at the accessory cell level.

We produced and characterized a panel of anti-HLA class II monoclonal antibodies (mAb) to study the inhibition of T cell-dependent B cell differentiation. The newly produced mAb belonged to different isotypes and subclasses, and recognized at least two different nonpolymorphic HLA class II determinants. We found that anti-HLA class II mAb inhibited the pokeweed mitogen (PWM)- and interleukin 2-driven T cell-dependent IgM synthesis, but did not affect the phorbol myristate acetate-, phytohemagglutinin-, anti-T3- or PWM-induced T cell proliferation. Moreover, when the mAb were tested in a monocyte-independent B cell differentiation assay in which T cells are activated by insoluble anti-T3 mAb in the absence of accessory cells, no effect was seen on IgM synthesis. These data indicate that inhibition of T cell-dependent B cell differentiation by anti-HLA class II mAb is caused by interference with an accessory cell function essential for B cell differentiation.

Antibodies, Monoclonal↗
PubMed1987

Xenogeneic recognition of soluble and cell surface HLA class II antigens by proliferative murine T cells.

In order to characterize the murine anti-human xenogeneic mixed lymphocyte reactions (MLR), we studied T cell proliferative responses against various human lymphoid cells by immunization of mice either with cellular or purified HLA-DR antigens. Data presented here indicated that small amounts of soluble HLA-DR antigen were able to prime mice, and that the xenogeneic MLR depends on the expression of HLA class II antigens on the stimulating cells. Experiments using a mutant cell line clearly showed that HLA-DP molecules were also sufficient in eliciting a primary or a secondary xenogeneic MLR while no secondary proliferative response was obtained with cells expressing only HLA class I molecules. Using a large panel of human cells with various haplotypes, our results also showed that (a) nonpolymorphic determinants of HLA class II antigens trigger dominantly the murine T cells and (b) the xenogeneic response required I-E and L3T4 accessory molecules and was not inhibited with anti I-A and monomorphic anti-HLA class II antigen monoclonal antibodies. Altogether these results suggest that HLA class II antigens act as nominal antigens in triggering a murine anti-human proliferative response.

Animals↗
PubMed1988

Alloantigen and microbial antigen-induced cellular immune responses: inhibitory effects of four anti-HLA class II monoclonal antibodies.

Four monoclonal antibodies (MAb's) directed against different epitopes of class II structures coded for by the human major histocompatibility complex (HLA), were studied to evaluate the relevance of these molecules on the control of different in vitro cell-mediated immune responses. Irrespective of the epitopes recognized, all MAb's tested exerted a powerful inhibitory effect on mixed lymphocyte cultures and on proliferation induced by microbial antigens. The generation of cytotoxic T lymphocytes and natural killer-like effectors also were inhibited by the addition of anti-HLA class II MAb in the cultures. The anti-HLA class II MAb provide a useful tool for the study of the in vitro immune response and eventually for therapeutic immunomodulation.

Antibodies, Monoclonal↗
PubMed1987

Altered expression of surface antigens with appearance of HLA class II molecules on a malignant human B-cell line.

Class II molecules of the major histocompatibility complex play an important role in mediating cellular interactions and are differentiation antigens on lymphobohematopoietic cells. We have previously characterized a human B-cell line (BALM-3) whose cells fail to express HLA class II molecules unless treated with phorbol acetate (TPA). Recently, we identified a spontaneous variant of BALM-3 whose cells express HLA class II molecules in the absence of TPA. Since normal B cells lose HLA class II molecules on terminal differentiation, these two BALM-3 cell populations may provide a model for a discrete phase of B-cell maturation. Alternatively, they may reflect two B-cell activation states characterized by quantitative differences in their expression of class II molecules. Expression of six of 22 additional surface molecules (HLA class I, CD23, p60, p124, p129, p141) increases by a factor of three or more as BALM-3 cells spontaneously acquire class II molecules while that of one of the 22 (p45) decreases by a comparable amount. Expression of the plasma cell-associated T10/CD38 antigen decreases by a factor of two. These additional surface molecules might also reflect lymphoid differentiation/activation antigens and/or participate in HLA class II-mediated cellular interactions and require further study. Use of TPA to induce the expression of HLA class II molecules produces similar changes in several but not all of these surface antigens.

Antigens, Neoplasm↗
PubMed1993

Ulcerative colitis: a genetically heterogeneous disorder defined by genetic (HLA class II) and subclinical (antineutrophil cytoplasmic antibodies) markers.

Newly described distinct associations of HLA class II genes with ulcerative colitis (UC) (DR2) and Crohn's disease (CD) (DR1/DQ5) provide strong evidence for genetic heterogeneity of susceptibility between these two forms of inflammatory bowel disease. A familial distribution of antineutrophil cytoplasmic antibodies (ANCAs, a subclinical marker of UC) in UC families has further implied the existence of heterogeneity within UC. To test the hypothesis that the heterogeneity within UC indicated by ANCAs has a genetic basis that resides within the HLA region, we studied 89 UC cases and an ethnically matched control group (n = 50). Serological and molecular typing techniques were applied to define HLA class II genes (DR, DQ). ANCAs were detected using an enzyme-linked immunosorbent assay, and positive values were confirmed by indirect immunofluorescence. We observed that ANCA-positive UC patients (n = 70) had a significantly increased frequency of DR2 compared with ANCA-negative controls (n = 46) (44% vs 22%, P = 0.01). In contrast, the frequency of DR2 in ANCA-negative UC cases (21%) was virtually identical to that in controls (22%, P = 0.9). Furthermore, the ANCA-negative UC patients had an increase in the DR4 allele compared with ANCA-positive UC (P = 0.004). Thus, with the combination of a subclinical marker (ANCAs) and molecular genetic markers, genetic heterogeneity has been demonstrated within UC: ANCA-positive UC associated with DR2, and ANCA-negative UC likely associated with DR4.

Adult↗
PubMed2001

The distribution of HLA class II susceptible/protective haplotypes could partially explain the low incidence of type 1 diabetes in continental Italy (Lazio region).

HLA class II is the primary susceptibility gene to type 1 diabetes and the analysis of HLA class II association could help to clarify the relative weight of genetic contribution to the incidence of the disease. Here we present an extensive typing for HLA class II alleles and their haplotypes in a homogenous population of type 1 diabetic patients (n=134) and controls (n=128) and in simplex (n=100) and multiplex families (n=50) from continental Italy (Lazio region). Among the various haplotypes tested, the DRB1*0301-DQA1*0501-DQB1*0201 was the most frequent found in type 1 diabetic patients and was transmitted in 82% of affected siblings, whereas DRB1*0402-DQA1*0301-DQB1*0302 appeared to have the highest odds ratio (10.4), this haplotype was transmitted in 96.3% of affected siblings, followed by DRB1*0405-DQA1*0301-DQB1*0302, DRB1*0405-DQA1*0301-DQB1*0201, DRB1*0401-DQA1*0301-DQB1*0302 and DRB1*0404-DQA1*0301-DQB1*0302. The following haplotypes showed a significant decreased transmission to diabetic siblings: DRB1*0701-DQA1*0201-DQB1*0303, DR2-DQA1*01-DQB1*0602, DR5-DQA1*0501-DQB1*0301. We suggest that the HLA DR/DQ haplotype/genotype frequencies observed could in part explain the low incidence of type 1 diabetes registered in Lazio region (8.1/100.000/year), for a number of reasons: i) the low frequency, in the general control population, of the most susceptible haplotypes and genotype for type 1 diabetes DRB1*0301-DQA1*0501-DQB1*0201 (14%), and DR4-DQA1*0301-DQB1*0302 (9%) and DRB1*0301-DQA1*0501-DQB1*0201/DR4-DQA1*0301-DQB1*0302 (0.8%) compared to other countries characterised by high incidence rate of the disease, Sardinia and Finland, respectively; ii) a significant lower ratio, in the control population, between the susceptible DRB1*0301-DQA1*0501-DQB1*0201 and the neutral DRB1*0701-DQA1*0501-DQB1*0201 haplotypes compared to the Sardinian population; iii) the high frequency of protection haplotypes/genotypes as the DR5-DQA1*0501-DQB1*0301, and DR5-DQA1*0501-DQB1*0301/DR5-DQA1*0501-DQB1*0301 very common in the control population of Lazio region and the DRB1*1401-DQA1*0101-DQB1*0503 haplotype.

Adolescent↗
PubMed1990

HLA class II typing by digestion of PCR-amplified DNA with allele-specific restriction endonucleases will fail to unequivocally identify the genotypes of many homozygous and heterozygous individuals.

Recently, a new technique for HLA class II genotyping has been introduced, the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method, claimed to be a practical alternative to conventional serological and cellular HLA class II typing (1-3). The PCR-RFLP technique is ingenious, relatively rapid and does not require hybridization with sequence-specific oligonucleotide probes. However, analysis of whether homozygous and heterozygous combinations of PCR-RFLP patterns for the various investigated HLA class II loci are unique or not unfortunately shows that only 19% of DRB homozygous and heterozygous combinations are unique. The figures for the DQA1, DQB and DPB loci are 56%, 29% and 65%, respectively. As not all nucleotide sequences analyzed in the above-mentioned studies (1-3) gave rise to unique PCR-RFLPs and as more sequences now are known, for the DRB1, DRB3, DRB5 and DPB1 loci (4), the frequencies of unique PCR-RFLP patterns for the different HLA class II loci will be reduced even further. Thus, the present analysis demonstrates that the PCR-RFLP technique, performed as described in references 1-3, is not yet ready to be used for routine HLA class II genotyping. The resolution of the PCR-RFLP method can be improved by various modifications. However, the role of a modified PCR-RFLP technique in HLA class II typing still remains to be shown.

Alleles↗
PubMed1992

Expression of HLA class II antigens on skin fibroblasts in scleroderma.

Skin biopsies were taken from 11 patients with morphoea, nine with acrosclerosis and 10 with diffuse systemic sclerosis and processed for immunohistochemical studies using a panel of monoclonal antibodies including antibodies to MHC class II antigens. A significantly higher percentage of HLA-DR positive dermal cells were observed in the reticular dermis in biopsies from patients with morphoea (44.1 +/- 16.2%), acrosclerosis (15.9 +/- 5.4%) and systemic sclerosis (39.5 +/- 2.3%) when compared with the controls (6.6 +/- 2%). A smaller percentage of dermal cells also expressed HLA-DP and -DQ. The degree of monocnuclear cell infiltrate in the biopsies, however, did not correlate with the percentage of HLA class II positive fibroblasts. In organ culture, the expression of the HLA class II antigens was almost totally lost after 3 days and was no longer detected on fibroblasts after 3 weeks of culture.

Cell Count↗
PubMedDate not supplied

Association between HLA class II antigens and hepatitis C virus infection.

The aim was to confirm the influence of HLA Class II antigens on the progression of HCV infection and to assess the relationship between these antigens and histological damage, HCV viral load and HCV genotype. 143 patients were enrolled and divided into three groups. Group A included 34 anti-HCV positive, HCV-RNA negative patients with ALT persistently normal; group B included 39 patients with HCV-RNA positive and abnormal ALT level; group C included 70 normal subjects. Serological HCL typing was performed with lymphocytotoxicity test by Terasaky and McClelland, using lymphobeads HLC class II. The frequency of HLA DR11 (5) was significantly higher in the control group (52.9%) and in group A (64.7%), than in group B (28.2%). Allele HLA DR6 was demonstrated in a similar proportion (26%) among control group and group B, while HLA DR14 (6) was less frequent among controls (18% vs 1.4%). In group A the frequency of HLA DR14 (6) was 3% compared to group B, HLA DR17 (3) was prevalent (15.4%) in group B. Liver damage was associated with the detection of HLA DR14 (6) and HLD DR17 (3) antigens. Significantly lower levels of HCV-RNA were measured in subjects with HLA DR11 (5) than in these with either DR6 or DR17 (3). HLA class II antigens appear crucial for resolution or progression of HCV hepatitis. The punctual identification of these genetic factors may, therefore, prove to be useful in predicting disease evolution, in guiding the appropriate therapy for patients with poor prognosis, and in encouraging the development of now therapeutic strategies.

Adult↗
PubMed2005

HLA class II restricted T-cell receptor gene transfer generates CD4+ T cells with helper activity as well as cytotoxic capacity.

Both cytotoxic T cells and helper T cells are important in immune responses against pathogens and malignant cells. In hematological malignancies which express HLA class II molecules, immunotherapy may be directed to HLA class II restricted antigens. We investigated whether it is possible to engineer HLA class II restricted T cells with both antigen-specific cytolytic activity and the capacity to produce high amounts of cytokines. CD4+ and CD8+ peripheral-blood-derived T cells were retrovirally transduced with the HLA class II restricted minor histocompatibility antigen dead box RNA helicase Y (DBY)-specific TCR. The TCR-transduced CD4+ T cells exerted DBY-specific cytolytic activity, produced Th0, Th1, or Th2 cytokines, and proliferated upon DBY-specific stimulation. TCR-transduced CD8+ T cells exerted cytolytic activity which equaled the level of cytolytic activity of the TCR-transferred CD4+ T cells. Cotransfer of CD4 enhanced the cytolytic activity of the TCR-transduced CD8+ T cells, but introduction of CD4 was not sufficient to generate DBY-specific CD8+ T cells with the capacity to produce high amounts of cytokines. In this study, we demonstrated the feasibility to engineer T cells with antigen-specific cytolytic activity, as well as the ability to produce significant amounts of cytokines, by TCR transfer to CD4+ T cells.

Cells, Cultured↗
PubMed1992

Synergism of glucocorticoids with granulocyte macrophage colony stimulating factor (GM-CSF) but not interferon gamma (IFN-gamma) or interleukin-4 (IL-4) on induction of HLA class II expression on human monocytes.

Peripheral blood monocytes from up to 13 normal donors were stimulated with the cytokines interferon gamma (IFN-gamma), interleukin 4 (IL-4) and granulocyte macrophage-colony stimulating factor (GM-CSF) in the presence or absence of dexamethasone (Dex), and the effects on HLA class II (HLA-DR, DP and DQ) expression studied. Dex markedly augmented HLA-DR, DP and DQ levels induced by GM-CSF, in all samples tested. Particularly striking were the effects on HLA-DQ expression, since stimulation with a combination of Dex and GM-CSF induced markedly higher levels of HLA-DQ antigen than stimulation with IFN-gamma. Northern blot analysis of samples treated for 40 hours with Dex and GM-CSF indicated that levels of DR alpha, DP alpha and DQ alpha mRNA were also increased. In contrast, despite variation between individual donors, in general Dex weakly inhibited both constitutive and IFN-gamma- or IL-4-induced HLA-DR expression. Variability in the responsiveness of monocytes purified from individual donors to each cytokine was also observed. GM-CSF was less potent than IFN-gamma and IL-4, enhancing HLA class II expression in only seven of 13 donors tested, whereas in the presence of Dex all donors responded to GM-CSF. The differential effects of glucocorticoids in vitro suggest that these cytokines induce HLA class II expression by different mechanisms.

Base Sequence↗
PubMed1999

HLA class II susceptibility to multiple sclerosis among Ashkenazi and non-Ashkenazi Jews.

OBJECTIVE: To look for HLA class II alleles and haplotypes conferring susceptibility to multiple sclerosis (MS) in the Jewish population of Israel. DESIGN: Population-based cohort of clinically definite patients with MS tested prospectively over 7 years. SETTING: Referral center in a neurology clinic at a university hospital in the greater Jerusalem area in Israel. PATIENTS: A total of 162 consecutive patients with clinically definite MS from the 2 main ethnic Jewish groups in Israel: 104 Ashkenazi (80 with a relapsing remitting or secondary progressive and 24 with a primary chronic progressive course of the disease) and 58 non-Ashkenazi (36 with a relapsing remitting or secondary progressive course and 22 with a primary chronic progressive course of the disease), matched with 132 Ashkenazi and 120 non-Ashkenazi healthy controls. MAIN OUTCOME MEASURES: The relationship between the various HLA class II alleles and haplotypes and MS, as defined by the polymerase chain reaction and sequence-specific oligonucleotide probe hybridization, among the Ashkenazi and the non-Ashkenazi Jewish sections and with respect to the different clinical courses of the disease. RESULTS: The haplotype DRB1*1501, DQA1*0102, DQB1*0602 was found to be associated with MS among both Ashkenazi and non-Ashkenazi patients (P<.001 and P =.04, respectively). Among the non-Ashkenazi patients, a new association of haplotypes DRB1*1303, DQA1*05, and DQB1*030 with MS was detected (P = .03). The MS susceptibility alleles, DRB 1* 1501, DQA1*0102, and DQB1*0602 , were found in association with the Ashkenazi patients (P<.001, P=.02, and P=.01, respectively); DRB1*1501 and DRB1*1303 were more frequently observed among the non-Ashkenazi patients (P = .03, P = .04, respectively). On subdivision of the patients into clinical subgroups, associations of DRB1*0801, DQA1*0102, DQA1*0401, and DQB1*0602 with primary chronic progressive MS among the Ashkenazi patients were evident (P = .03, P = .04, P = .04 and P = .05, respectively), whereas DRB1* 1501, DRB1*03011, and DQB1*0602 were associated with relapsing remitting or secondary progressive among the non-Ashkenazi patients (P = .05, P = .05, and P = .03, respectively). CONCLUSIONS: This study, unlike previous ones, is the first to show a significant association between HLA class II alleles and MS in the Jewish population. The association with the HLA-DR2-related haplotype is similar to that among non-Jewish white patients with MS. Moreover, our data support the possibility that DRB1*1501 is the susceptibility allele responsible for the association between this haplotype and MS in the Jewish population. Our study also underscores differences in HLA profiles between Ashkenazi and non-Ashkenazi patients, and between the different clinical courses of the disease. The latter may indicate that the clinical courses of MS are influenced by the genetic background.

Alleles↗
PubMed2000

Association of antiphosphatidylserine/prothrombin autoantibodies with HLA class II genes.

OBJECTIVE: To investigate the associations between HLA class II genes and antiphosphatidylserine/prothrombin antibodies (aPS/PT) in a group of British caucasoid patients with antiphospholipid antibodies (aPL). METHODS: This study included 82 patients with aPL. IgG aPS/PT were detected in sera using enzyme-linked immunosorbent assays. HLA-DQB1, DQA1, and DRB1 genotypes were determined by polymerase chain reaction using sequence-specific primers. All results were compared with 177 matched healthy control subjects. RESULTS: IgG aPS/PT were present in 41 of 82 patients (50%). The frequencies of DQB1*0301/4, DQB1*0604/5/6/7/9, and DRB1*1302 alleles were increased in patients with aPS/PT compared with controls. To minimize the interference of the association between anti-beta2-glycoprotein I (anti-beta2GPI) and HLA, patients with anti-beta2GPI were excluded from further analyses, and only HLA-DQB1*0301/4 remained significant compared with controls (odds ratio [OR] 2.75, 95% confidence interval [95% CI] 1.2-6.5, P < 0.03). In the haplotype analysis, HLA-DQB1*0301/4;DQA1* 0301/2;DRB1*04 was significantly increased in patients with IgG aPS/PT compared with controls (OR 4.75, 95% CI 1.72-13.10, P = 0.0063). CONCLUSION: The HLA-DQB1*0301/4;DQA1*0301/ 2;DRB1*04 haplotype and its components may influence the production of aPS/PT in the antiphospholipid syndrome, which partly explains the correlation between the lupus anticoagulant and DQB1*03.

Adolescent↗
PubMed2000

HLA class II alleles in Japanese patients with immune thrombocytopenic purpura. Associations with anti-platelet glycoprotein autoantibodies and responses to splenectomy.

HLA class II alleles and immunoglobulin allotypes were determined in 83 Japanese patients with immune thrombocytopenic purpura (ITP) and 114 race-matched healthy controls. Distribution of DRB and DQB1 alleles as well as G1M(f, z), G2M(n+, n-), and KM(1, (1,2), 3) were not different between ITP patients and healthy controls, while DPB1*0201 was marginally increased in ITP patients vs. healthy controls (51% vs. 28%, Pc= 0.04, OR=2.6 [1.4-4.8]). In contrast, strong associations between anti-glycoprotein autoantibodies and HLA class II genes were found as follows: antiGPIIb-IIIa antibody with DRB1*0405 and DQB1*0401; and anti-GPIb-IX antibody with DRB1*0803 and DQB1*0601. When factors influencing therapeutic responses to splenectomy were examined, a poor response was correlated with the presence of DRB1*0405, DQB1*0401 and anti-GPIIb-IIIa antibody (P=0.01, 0.002, and 0.03, respectively). Our results indicate that HLA class II genes influence the production of anti-glycoprotein antibody specificities rather than the development of ITP. In addition, HLA class II genotyping could be useful in predicting therapeutic responses to splenectomy in Japanese patients with ITP.

Adult↗
PubMedDate not supplied

Langerhans cell and HLA class II molecules distribution in lung carcinoma.

We have evaluated Langerhans cell (LC) distribution in 19 lung carcinomas and 1 carcinoid tumor, furthermore investigating HLA class II molecules expression by the neoplastic cells; this was done using, in immunohistochemical tests, a polyclonal antiserum anti S-100 protein for the identification of LCs and a mouse Monoclonal Antibody (MoAb) for the detection of HLA class II -DR molecules. Our results indicate that LCs are poorly represented in lung carcinomas and likewise HLA class II molecules are scarcely expressed by the neoplastic cells; this might be important in understanding the ominous prognosis of lung carcinomas since both parameters investigated play a central role in the immune response against human neoplasia, LCs as antigen presenting cells and HLA class II molecule as restriction elements during antigen stimulation of CD4+ T lymphocytes.

HLA-DR Antigens↗
PubMed1996

Vitamin D3 reduces the apoptotic effect of IFN-gamma but does not facilitate HLA class II inducibility in RB-defective cells.

The retinoblastoma protein (RB) regulates the cell cycle by binding and inactivating the E2F transcription factors, which prevents transcription of genes required for DNA synthesis. RB has been shown to inhibit IFN-gamma-mediated apoptosis, possibly by regulating premature entry into S phase. RB is also required for high level IFN-gamma induction of HLA class II genes, which encode antigen presenting molecules, but not for other IFN-gamma inducible genes as demonstrated in previous reports describing the analysis of RB-transformants of the RB-defective cell lines, MDA-468-S4 (S4) and H2009. The IFN-gamma response of the HLA class II genes takes much longer than does the response of the other IFN-gamma inducible genes, raising the question of whether RB facilitates HLA class II inducibility by maintaining cell viability over the long time course required for HLA class II induction. Thus, we sought to learn whether IFN-gamma induced apoptosis in an RB-defective cell line could be prevented independently of RB and whether doing so would facilitate HLA class II inducibility in the RB-defective line. Our results indicated that cotreating the RB-defective S4 cells with IFN-gamma and Vitamin D3 decreased the number of cells containing subdiploid DNA compared to cells treated with IFN-gamma alone, suggesting that Vitamin D3 reduced IFN-gamma-mediated apoptosis. S4 cells cotreated with Vitamin D3 and IFN-gamma also had decreased cell detachment, further indicating that Vitamin D3 decreased IFN-gamma induced apoptosis. However, Vitamin D3 cotreatment resulted in no detectable increase in HLA-DR, the most prominent HLA class II molecule, indicating that the effect of RB on HLA class II induction is not exclusively due to its ability to inhibit IFN-gamma induced apoptosis.

Apoptosis↗