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Biomedical subjects

Jianming Tang

Publications and source records attributed to Jianming Tang.

At least 19 recordsLinked to original sources

Ionizing radiation induces bidirectional transcriptomic reprogramming and dynamic NOS2/TREM2 regulation in triple-negative breast cancer cells.

PURPOSE: To characterize irradiation-associated transcriptomic changes in murine triple-negative breast cancer cells and examine dose- and time-response patterns of selected radiation-responsive candidates. MATERIALS AND METHODS: RNA sequencing (RNA-seq) was performed in 4T1 cells collected 24 h after 4 Gy irradiation, followed by Reactome and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment and gene set enrichment analyses. Representative RNA-seq-derived genes were examined by reverse transcription quantitative PCR (RT-qPCR), and selected immune- and inflammation-related transcripts were further assessed across additional radiation doses and post-irradiation time points. Inducible nitric oxide synthase (NOS2) and triggering receptor expressed on myeloid cells 2 (TREM2) protein abundance was assessed by Western blotting, and nitrite accumulation in culture supernatants was measured using a Griess reagent-based assay as an indirect readout of nitric oxide production. RESULTS: RNA sequencing identified 757 differentially expressed genes, including 285 upregulated and 472 downregulated genes. Irradiation was associated with enrichment of inflammatory, interferon-related, immune-system, and cell-adhesion transcriptional signatures, whereas downregulated genes were enriched in cell-cycle-, chromosome-cohesion-, DNA-damage-response-, DNA-repair-, and SUMOylation-related pathways. Selected immune- and inflammation-related transcripts showed distinct temporal patterns. Nos2 mRNA increased across the examined 0-6 Gy dose range and at later post-irradiation time points, whereas NOS2 protein showed different kinetics, with an early peak after 4 Gy irradiation and no clear further increase above 6 Gy. Nitrite accumulation increased after irradiation. Trem2 showed the largest fold increase among strongly upregulated transcripts identified by RNA-seq, but RT-qPCR detected a significant increase only at 24 h, and TREM2 protein abundance remained unchanged across the examined doses and time points. CONCLUSIONS: Ionizing radiation was associated with broad bidirectional transcriptional remodeling in 4T1 cells, involving immune-, inflammatory-, and interferon-related signatures together with reduced representation of cell-cycle- and DNA-repair-related gene sets. The discordant mRNA and protein patterns of NOS2 and TREM2 indicate that transcript-level responses do not necessarily translate into corresponding protein-level changes. These findings define irradiation-associated molecular responses requiring further functional investigation.

Triple-negative breast cancer↗

Cohort- and time-specific associations of CTLA4 genotypes with HIV-1 disease progression.

BACKGROUND: CTLA4 in the chromosome 2q33 region encodes cytotoxic T-lymphocyte (CTL) associated antigen 4, which downregulates CTL responses. We examined the relationships between common CTLA4 variants and several outcomes of HIV-1 infection in adults and adolescents. METHODS: We studied 765 HIV-1-infected persons: 558 Caucasian seroconverters from three cohorts (MACS, ACS, and DCG) and 207 infected adolescents (mostly female) from another cohort (REACH) of mixed ethnicity. Single nucleotide polymorphisms in CTLA4 promoter (-1147C/T, -658C/T, -318C/T), coding sequence (49A/G) and the 3' untranslated region (CT60A/G) were resolved by PCR-based techniques. Repeated measures and survival analyses were used to test allelic and haplotypic associations with HIV-1 viral load (VL) and time to AIDS, respectively. RESULTS: Individuals carrying -318T or the (-1147) T-(-318) T haplotype had elevated HIV-1 VL in MACS and REACH but reduced VL in DCG and ACS participants. Time-dependent associations of CTLA4-318T with VL were observed in MACS and REACH (P = 0.03-0.09). In Cox regression models adjusted for age and established contributory markers in CCR5 and HLA class I genes, CTLA4-318T was associated with rapid progression to AIDS in MACS (relative hazard 1.69; 95% confidence interval, 1.15-2.49; P < 0.01) as opposed to a non-significant slower disease progression in ACS and no appreciable association in DCG. CONCLUSIONS: Association of CTLA4 genotypes with clinical and virological outcomes following HIV-1 infection appeared to vary with time and among the cohorts. Further analyses in conjunction with other biologically and positionally related genes, such as CD28 and ICOS, may help explain the disparate findings.

Acquired Immunodeficiency Syndrome↗

Human leukocyte antigen B58 supertype and human immunodeficiency virus type 1 infection in native Africans.

Human leukocyte antigen (HLA) class I alleles can be grouped into supertypes according to their shared peptide binding properties. We examined alleles of the HLA-B58 supertype (B58s) in treatment-naïve human immunodeficiency virus type 1 (HIV-1)-seropositive Africans (423 Zambians and 202 Rwandans). HLA-B and HLA-C alleles were resolved to four digits by a combination of molecular methods, and their respective associations with outcomes of HIV-1 infection were analyzed by statistical procedures appropriate for continuous or categorical data. The effects of the individual alleles on natural HIV-1 infection were heterogeneous. In HIV-1 subtype C-infected Zambians, the mean viral load (VL) was lower among B*5703 (P = 0.01) or B*5703-Cw*18 (P < 0.001) haplotype carriers and higher among B*5802 (P = 0.02) or B*5802-Cw*0602 (P = 0.03) carriers. The B*5801-Cw*03 haplotype showed an association with low VL (P = 0.05), whereas B*5801 as a whole did not. Rwandans with HIV-1 subtype A infection showed associations of B*5703 and B*5802 with slow (P = 0.06) and rapid (P = 0.003) disease progression, respectively. In neither population were B*1516-B*1517 alleles associated with more favorable responses. Overall, B58s alleles, individually or as part of an HLA-B-HLA-C haplotype, appeared to have a distinctive impact on HIV-1 infection among native Africans. As presently defined, B58s alleles cannot be considered uniformly protective against HIV/AIDS in every population.

Africa↗

Association between human leukocyte antigen class II alleles and genotype of Borrelia burgdorferi in patients with early lyme disease.

BACKGROUND: On the basis of a polymerase chain reaction-restriction fragment-length polymorphism analysis of the 16S-23S ribosomal DNA intergenic spacer, clinical isolates of Borrelia burgdorferi can be classified into 3 genotypes designated as RST1, RST2, and RST3. RST1 strains are the most pathogenic, and RST3 strains are the least pathogenic. METHODS: Human leukocyte antigen (HLA) class II alleles were determined for a group of culture-positive patients with Lyme disease-associated erythema migrans and were evaluated for an association with the genotype of the infecting B. burgdorferi strain. RESULTS: The DRB1*0101 allele carriage rate was higher in patients infected with RST3 strains (9/25 [36.0%]) than in patients infected with RST1 strains (2/28 [7.1%]) or RST2 strains (7/36 [19.4%]) (P=.010). The same relationship was found for carriage of the DRB1*0101-DQB1*0501 haplotype (P=.018), because of tight linkage disequilibrium. Similar associations could not be demonstrated for any of the other DRB1 and DQB1 alleles or haplotypes that were assessed. CONCLUSION: The DRB1*0101 allele and the DRB1*0101-DQB1*0501 haplotype may be relevant to the development of infection with strains from the least invasive genotypes of B. burgdorferi.

Adult↗

A case-control study to examine HLA haplotype associations in patients with posttreatment chronic Lyme disease.

In a comparison of 95 patients with systemic symptoms that persisted after antibiotic treatment for acute Lyme disease (posttreatment chronic Lyme disease) and 104 control subjects without such symptoms after antibiotic treatment, we sought associations between human leukocyte antigen class II (DRB1 and DQB1) markers and posttreatment chronic Lyme disease. No strong association between posttreatment chronic Lyme disease and any class II allele or genotype was found.

Adult↗

Human leukocyte antigen and cytokine gene variants as predictors of recurrent Chlamydia trachomatis infection in high-risk adolescents.

Antigen presentation and immune activation are essential to the effective control of infectious diseases. In 485 North American adolescents at high risk for genital Chlamydia trachomatis infection, we found 2 human leukocyte antigen variants (DRB1*03-DQB1*04 and DQB1*06) to be associated with recurrent Chlamydia infection (adjusted relative odds [RO], >2.0; P<.01, for both variants). A G-C-C haplotype corresponding to variants at IL10 (encoding interleukin-10 [IL-10]) promoter positions -1082, -819, and -592 was underrepresented in individuals with recurrent infection (RO, 0.59; P=.046). These genetic associations were independent of nongenetic factors, including number of sex partners, race, sex, duration of follow-up, and human immunodeficiency virus type 1 seropositivity. Consistent with the observed IL10 association, cervical secretions in female adolescents without the IL10 G-C-C haplotype had elevated IL-10 concentrations after Chlamydia infection, which may reflect involvement of a Chlamydia-specific mechanism for genetically mediated, differential IL-10 expression in the genital tract.

Adolescent↗

HLA-B, -DRB1/3/4/5, and -DQB1 gene polymorphisms in human immunodeficiency virus-related Kaposi's sarcoma.

Polymorphisms of genes in the human leukocyte antigen (HLA) complex, particularly those encoding HLA-DR, have been suggested as markers of susceptibility to Kaposi's sarcoma (KS). We conducted a case-control study comparing 147 homosexual men who developed KS after infection by human immunodeficiency virus-1 (HIV-1) and human herpes virus 8 (HHV8) with 147 matched dually infected men without HIV-associated KS (HIV-KS) from the Multicenter AIDS Cohort Study. HLA-B, DRB1, DRB3, DRB4, DRB5, and DQB1 polymorphisms were examined by high-resolution DNA-based methods. Differences in distributions of genetic variants were tested by conditional logistic regression. Previously reported relationships with HLA-DRB1 alleles could not be confirmed. Instead, other associations were observed. In univariate analysis, KS was weakly associated with B*2702/5 (odds ratio (OR)=0.40, 95% confidence interval (CI)=0.18-0.91). Similar or stronger associations, positive or negative, were seen for haplotypes containing class II alleles: DRB1*1302-DQB1*0604 (OR=3.67, 95% CI=1.02-13.1), DRB4 (DR53) haplotype family members [OR=0.52, 95% CI=0.32-0.85], and DRB3 (DR52) haplotype family members (OR=1.69, 95% CI=1.07-2.67). The B*1402-DRB1*0102 haplotype, which invariably contains the V281L mutation in the 21-hydroxylase gene governing adrenal steroid biosynthesis, occurred in five cases and one control (OR=5.0, 95% CI=0.58-42.8). In a final multivariable analysis, only DRB1*1302-DQB1*0604 (OR=6.43, 95% CI=1.28-32.3, P=0.02) remained significantly associated with KS. Associations of HLA-DRB families with HIV-KS could reflect underlying immune dysregulation. The HLA B*1402-DRB1*0102 haplotype associated with increased risk of KS might represent an antigen-presenting pathway unfavorable for immune response to HHV8. Alternatively, the relationship might hold a clue to the predilection of KS for men because that haplotype harbors the mutant form of the 21-hydroxylase gene.

Case-Control Studies↗

Positive and negative associations of human leukocyte antigen variants with the onset and prognosis of adult glioblastoma multiforme.

Associations of genetic factors with malignant gliomas have been modest. We examined the relationships of human leukocyte antigen (HLA) and related polymorphisms to glioblastoma multiforme in adult Caucasians (non-Hispanic Whites) from the San Francisco Bay area. For 155 glioblastoma multiforme patients and 157 control subjects closely matched by ethnicity, age, and gender, PCR-based techniques resolved alleles at HLA-A, -B, -C, and -DRB1 loci along with short tandem repeat polymorphisms of MICA exon 5 and TNFb. By multivariable logistic regression, B*13 and the B*07-Cw*07 haplotype were positively associated with glioblastoma multiforme (P=0.01 and <0.001, respectively), whereas Cw*01 was the only variant showing a negative association (P=0.05). Among glioblastoma multiforme patients, progression to death after diagnosis was slower in those with A*32 (relative hazard, 0.45; P<0.01) and faster in those with B*55 (relative hazard, 2.27; P<0.01). Thus, both the occurrence and the prognosis of glioblastoma multiforme could be associated with specific but different HLA genotypes. B*07 and the B*07-Cw*07 haplotype are much more common in Caucasians than other ethnic groups in the U.S., which may partially explain the higher incidence of glioblastoma multiforme in Caucasians.

Adult↗

Epidemiological and genetic correlates of incident Chlamydia trachomatis infection in North American adolescents.

Epidemiological and genetic correlates of Chlamydia trachomatis infection were examined prospectively in 124 male and 361 female adolescents at high risk for human immunodeficiency virus type 1 (HIV-1) infection. Seventy percent of subjects were African American, and 68% had HIV-1 infection. As expected, younger age (<17 years), multiple sex partners (> or =2), and prior chlamydial infection predicted chlamydial infection during a 6-56-month follow-up period (P=.02, P=.02, and P=.03, respectively). Human leukocyte antigen (HLA) class II variant DQB1*06 (mostly *0602 and *0603) was associated with chlamydial infection (49% vs. 34%; adjusted relative odds [RO], 1.8; P=.005), as was HLA class I haplotype B*44-Cw*04 (10% vs. 4%; RO, 3.2; P=.009). DQB1*06 was found in 9 (75%) of 12 female adolescents with chlamydial pelvic inflammatory disease. In contrast, sex, ethnicity, and HIV-1 infection did not predict chlamydial infection. These findings suggest that antigen presentation in adaptive immune responses may serve as a major factor in effective control of C. trachomatis infection. The underlying mechanisms remain to be experimentally elucidated.

Adolescent↗

Transmission of HIV-1 and HLA-B allele-sharing within serodiscordant heterosexual Zambian couples.

Factors that might increase risk of HIV-1 transmission include age, sex, and amount of HIV-1 RNA in plasma, but findings for HLA allele-sharing are not in agreement. We tested the hypothesis that allele sharing at HLA loci is associated with increased risk of transmission of HIV-1 infection in cohabiting heterosexual Zambian couples. We studied 125 initially serodiscordant partners with sequence-confirmed interpartner HIV-1 transmission and 104 couples who were persistently serodiscordant, and we analysed relations with molecularly typed HLA-A, B, and C alleles by survival techniques. After adjustment for other genetic and non-genetic risk factors seen with heterosexual transmission of HIV-1 in this cohort, sharing of HLA-B alleles was independently associated with accelerated intracouple transmission (relative hazard 2.23, 95% CI 1.52-3.26, p<0.0001). Selective pressure by HLA-B alleles on transmitted viruses accords with current understanding of the effect of B locus polymorphism in HIV-1 and perhaps other infections.

Adult↗

HLA-DRB1 and -DQB1 alleles and haplotypes in Zambian couples and their associations with heterosexual transmission of HIV type 1.

In 292 initially human immunodeficiency virus (HIV)-1-serodiscordant and cohabiting Zambian couples, HLA-DRB1 and -DQB1 variants were associated with HIV-1 transmission events during a 7-year follow-up period. Initially seronegative partners with either DRB1*0301-DQB1*0201 (relative hazard [RH], 1.60; P=.009) or DRB1*1503-DQB1*0602 (RH, 1.67; P=.03) showed accelerated seroconversion. Carriage of DRB1*1301 in initially seropositive partners led to delayed transmission of HIV to their spouses (RH, 0.54; P=.05). The combined groups of seroprevalent and seroincident partners (n=433) also differed from those who remained seronegative (n=151), with regard to 2 common haplotypes, DRB1*1302-DQB1*0604 (relative odds [RO], 0.28; P=.003) and DRB1*1503-DQB1*0602 (RO, 1.81; P=.02). Statistical adjustments for other host factors (age, sex, genital ulcer, and index partner's virus load) known to influence transmission of HIV-1 seldom altered the genetic relationships. Overall, associations of HLA class II polymorphisms with both HIV transmission and acquisition are not as readily interpretable as are effects reported for other loci.

Adult↗

Cytokine and chemokine gene polymorphisms among ethnically diverse North Americans with HIV-1 infection.

Twenty-four common single nucleotide polymorphisms (SNPs) in 10 cytokine and chemokine genes were defined in 579 North Americans at high risk of HIV-1 infection due to sexual behavior and injection drug use. Among the 3 major ethnic (African-American, Hispanic/Latino, and other) groups involved, HIV-1-seropositive individuals differed significantly from ethnically matched HIV-1-seronegative individuals (odds ratios = 2.13-4.82; P = 0.003-0.05) for several SNPs and haplotypes defined at the IL4, IL4R, IL6, IL10, CCL5 (RANTES), and CXCL12 (SDF1) loci. In addition, the homozygous IL4-590T/T genotype was associated with higher (+87-131 cells/microL) CD4 T-cell counts in HIV-1-infected and AIDS-free adolescents not receiving antiretroviral therapy (adjusted P = 0.004). No SNPs at IFNG, IL2, IL12B, TNF, or CCL2 (MCP1) showed any association with HIV-related outcomes. Additional typing for IL1A, IL1B, IL1R1, IL1RN, and TGFB1 SNPs also failed to demonstrate any influence on HIV-1 infection or virologic/immunologic control in more selected patient groups. Coupled with previous findings, our data suggest that heritable IL4 and IL10 variations may contribute to the acquisition or progression of HIV infection and that the effects of other targeted loci in the cytokine and chemokine system cannot be established unequivocally in the study populations.

Adolescent↗

HLA and cytokine gene polymorphisms are independently associated with responses to hepatitis B vaccination.

Variable immune responses to hepatitis B virus (HBV) infection and recombinant HBV vaccines have been associated with polymorphisms in several genes within the human leukocyte antigen (HLA) complex. Analyses of polymerase chain reaction (PCR)-based genotyping data from 164 North American adolescents vaccinated with recombinant HBV products confirmed that HLA-DRB1*07 (relative odds [RO] = 5.18, P <.0001) and human immunodeficiency virus type 1 (HIV-1) infection (RO = 3.91, P <.001) were both associated with nonresponse to full-dose vaccination. Further associations were observed with single nucleotide polymorphisms (SNPs) at the IL2 and IL4 loci along with insertion/deletion variants at the IL12B locus (P =.003-.01). Host genetic associations were independent of one another as well as other HLA (A, B, C, and DQB1) and cytokine gene (IL4R, IL6, IL10, and TNF) variants. Statistical adjustments for nongenetic factors (gender, ethnicity, age, HIV-1 infection, and vaccination protocols) did not substantially alter the strengths of the genetic relationships. The overall distribution pattern of genetic variations was similar between the analyzed vaccinees and additional adolescents (n = 292) from the same cohort. In conclusion, DRB1*07 (or a closely linked allele) and immunoregulatory cytokine gene polymorphisms correlate with variable immune response to recombinant HBV vaccines.

Cohort Studies↗

HLA allele sharing and HIV type 1 viremia in seroconverting Zambians with known transmitting partners.

Rapid HIV type 1 (HIV-1) mutation coupled with immune evasion poses a major obstacle to effective interventions. In particular, transmission of HIV-1 from a donor partner (transmitter) to a recipient (seroconverter) with similar antigen-presenting molecules (i.e., human leukocyte antigens, HLA) may favor or expedite viral adaptation to host immune responses. Our PCR-based HLA-A, HLA-B, and HLA-DRB1 genotyping for 115 Zambian couples with documented intracouple HIV-1 (mostly clade C) transmission revealed that single-locus HLA allele sharing ranged from 28 to 36%. Different degrees of allele sharing, at single or multiple HLA loci between donor-recipient pairs, were associated with only modest increases in seroconverter RNA level (+0.04 to + 0.24 log(10) copies/mL, p > 0.25). Thus, partial HLA allele sharing commonly seen in Zambian couples did not appear to confer unequivocal early advantage for viral replication in the newly seroconverting subjects. However, correlation of virus loads in seroconverters with those of their known index partners (adjusted Pearson r = 0.21, p = 0.03) did imply that viral characteristics can independently contribute to variability in plasma virus load.

Adult↗

Influence of human leukocyte antigen-B22 alleles on the course of human immunodeficiency virus type 1 infection in 3 cohorts of white men.

The human leukocyte antigen (HLA)-B22 serogroup--which consists of the alleles B*54, B*55, and B*56--has been associated with rapidly progressive disease in white patients with human immunodeficiency virus (HIV) infection. Subjects from 3 cohorts of men who have sex with men (N=671), all of whom experienced HIV-1 seroconversion at roughly the same time, were molecularly typed at HLA-A, -B, and -C loci. Mean HIV RNA loads during early HIV infection were higher in B22-positive men than in B22-negative men (difference, 0.481 log(10) HIV RNA copies/mL; 95% confidence interval [CI], 0.156-0.806 log(10) HIV RNA copies/mL; P=.004). Independent of accepted markers of progression, time-to-AIDS was shorter in B22-positive seroconverters (adjusted hazard ratio, 1.98; 95% CI, 1.27-3.10; P=.003). White B22 serogroup alleles (B*55 and *56) appear to predispose to unfavorable outcome of HIV infection as strongly as some or all B*35 and B*53 alleles. This finding may have greater implications for Asians, because the marker frequency for B22 is higher among Asians than among whites (approximately 10% vs. approximately 4%).

Adult↗

Cross-reactive CD8+ T cell epitopes identified in US adolescent minorities.

Vaccines designed to bring forth CD8+ T cell responses in different racial and ethnic groups will require inclusion of T cell epitopes presented by various MHC class I molecules. This study was designed to identify new CD8+ T cell epitopes in HIV-infected African American and Hispanic youth as well as to determine the frequency of responses to both novel and previously described HIV-1 epitopes in a cohort of racially and ethnically diverse individuals. We found 8 MHC class I-restricted CD8+ T cell epitopes that had not been previously described, another 8 epitopes that were restricted by class I alleles not previously associated with these epitopes, and 8 additional epitopes that have been described previously. In a larger cohort, we demonstrated that 11 (69%) of these 16 newly described immunogens were recognized by individuals of different race or ethnicity. Most HIV-1-specific CD8+ T cell epitopes identified were either novel or restricted by alternative MHC class I alleles. Frequent recognition of several of these CTL epitopes in persons of diverse racial backgrounds bodes well for the development of a broadly reactive HIV-1 vaccine.

AIDS Vaccines↗

The complexity of HLA class II (DRB1, DQB1, DM) associations with disseminated Mycobacterium avium complex infection among HIV-1-seropositive whites.

Earlier associations of polymorphism in classic HLA class II (DRB1 and DQB1) genes have been extended to include the accessory genes DMA and DMB as determinants of disseminated Mycobacterium avium complex (DMAC) infection among HIV-1-seropositive whites. From the Multicenter AIDS Cohort study, 176 DMAC cases were matched with 176 controls in a nested case-control study. PCR-based HLA genotyping techniques were used to resolve variants of DRB1 and DQB1 to their four-digit or five-digit alleles, and single-strand conformation polymorphism was used to resolve sequences in exon 3 at each DM locus. The DMA*0102 allele occurred less frequently among DMAC cases than among controls (OR = 0.46, p =.02). Combinations of DRB1 alleles with or without specific DMA and DMB variants showed significant differences in distributions between the cases and controls, but both of the previously associated class II alleles (DRB1*1501 and DRB1*0701) showed stronger positive associations with DMAC in the absence than in the presence of DMA*0102. Apparent joint effects of DRB1 and DM allelic combinations on occurrence and timing of DMAC suggest that class II disease relationships may be better predicted by biologically plausible interactive combinations than by polymorphisms in individual genes.

AIDS-Related Opportunistic Infections↗

Association of CTLA4 polymorphisms with sustained response to interferon and ribavirin therapy for chronic hepatitis C virus infection.

Cytotoxic T lymphocyte antigen-4 (CTLA4) suppresses cytotoxic T lymphocyte activity. We examined the associations of CTLA4 single-nucleotide polymorphisms (SNPs) at promoter site -318 and exon-1 site 49 with clearance of hepatitis C virus (HCV) after treatment with combination interferon-alpha plus ribavirin (IFN-alpha+R) therapy in 79 white sustained responders (SRs) and 79 nonresponders (NRs). SRs had higher frequencies of 49G, alone (odds ratio [OR], 2.3; P=.042) and tightly linked with -318C in a haplotype (OR, 2.4; P=.030). Homozygosity for the -318C-49G haplotype was even more frequent among SRs (OR, 5.2; P=.049). Comparably strong associations persisted after multivariable analysis. Relationships were not seen with non-1 genotype viruses (OR, 0.93-1.25; P>.25). Virus load also declined more rapidly in carriers of both 49G (P=.0095) and the -318C-49G haplotype. CTLA4 49G in exon 1 alone and in a haplotype with -318C promoter is associated with sustained IFNalpha+R response in white patients with HCV genotype 1 infection.

Abatacept↗