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W M Collins

Publications and source records attributed to W M Collins.

At least 19 recordsLinked to original sources
PubMed1995

B-complex recombinants and sarcoma regression: role of B-L/B-F region genes.

The anti-sarcoma response of three B complex recombinant haplotypes BR1(F24-G23), BR2(F2-G23), and BR3(F2-G23) was investigated. In a preliminary experiment, one male heterozygous for the BR1 recombinant haplotype and another heterozygous for the BR2 recombinant haplotype were each mated to females, some of which carried the respective recombinant. The anti-sarcoma response of progeny carrying the BR1 recombinant differed significantly from that of progeny carrying the BR2 recombinant. Subsequently, each of the three recombinant haplotypes was placed on each of four B haplotype complex backgrounds, and compared to B-G and B-L/B-F region controls on the same background haplotype. For each recombinant, significant differences in tumor growth were found between the recombinant and B-L/B-F control chickens on either one, two, or three of the four genetic backgrounds tested. For each recombinant, no differences were found between chickens carrying the recombinant and B-G region controls, which is further evidence that the gene(s) controlling Rous sarcoma growth lies in or near the B-L/B-F chromosomal region. Moreover, although the BR2 and BR3 recombinants appear to be identical serologically, they differed significantly in tumor growth suggesting that the two haplotypes are genetically different.

Animals↗
PubMed1993

Influence of different B-complex recombinants on the outcome of Rous sarcomas in chickens.

Seven major histocompatibility (B) complex recombinants were evaluated for anti-Rous sarcoma response. In experiment 1, the BR5(F21-G19) recombinant haplotype both homozygous and in heterozygous combinations with B19 and B21 haplotypes were compared to B19/B19 and B21/B21 chickens to determine the relative influence of the BF versus BG chromosomal segments on regression of Rous sarcoma virus-induced tumours. In experiment 2, six recombinant haplotypes BR1(F24-G23), BR2(F2-G23), BR3(F2-G23), BR4(F2-G23), BR6(F21-G23) and BR8(F2-G2a,23) present in chickens heterozygous for normal haplotypes B19, B23 or B26 were compared for anti-sarcoma response. A total of 1328 chickens were blood typed for B alloantigens at 17 days of age, inoculated in the wingweb with Rous sarcoma virus at 6 weeks and monitored for anti-tumour immune response over a 10-week period. Genotypes which shared the same BF haplotype, but differed in their BG regions, had similar anti-tumour responses, implicating the BF but not the BG region in tumour regression. Chickens carrying BF2 or BF21 had a strong anti-tumour response, while BF24 conferred a weaker response, regardless of the accompanying normal haplotype.

Animals↗
PubMed1987

Influence of the major histocompatibility complex on tumor regression and immunity in chickens.

A number of studies show that major histocompatibility complex (MHC) genes control host immune responses to viral-induced chicken tumors. The MHC gene-controlled responses to malignant neoplasms caused by Rous sarcoma virus, lymphoid leukosis virus and Marek's disease virus are reviewed. Genes that determine regression of Rous sarcomas and resistance to development of lethal Marek's disease lymphomas appear to map within the B-F region of the MHC. In some cases, genetic complementation of both MHC genes and non-MHC genes may be responsible for regression of tumors. Metastasis of Rous sarcoma cells is also influenced by the host's MHC genotype. Background genes can modify the specific MHC gene effect on resistance to progressive growth of Rous sarcomas and Marek's disease lymphomas. Studies showing that MHC-restricted immunity may be important in cytotoxic T cell reactions to virus-infected and/or transformed chicken cells are discussed. The MHC-restricted cytotoxicity, whereby the T cells and target cells must share one MHC haplotype for in vitro killing to occur, suggests that the T cells have receptors that recognize virus-altered self MHC antigens. This may be an important immune surveillance mechanism for limiting the proliferative growth of virus-induced tumors in chickens.

Animals↗
PubMed1986

Genetic interaction between non-MHC T- and B-cell alloantigens in response to Rous sarcomas in chickens.

Chickens of Regional Poultry Research Laboratory (RPRL) inbred line 6(3) regress sarcomas induced by Bryan high-titer Rous sarcoma virus to a greater extent than chickens of line RPRL 100, although these lines are identical for the major histocompatibility B complex. They differ, however, at three independent autosomal loci: Ly-4 and Th-1 determine the surface alloantigens of partly overlapping subsets of T lymphocytes, and Bu-1 determines a surface alloantigen of B lymphocytes. The association of genotypes at these loci with quantitative variation in their ability to regress Rous sarcomas was tested in segregating F4 generation progeny derived from crosses of lines 100 and 6(3). The Ly-4 and Bu-1 genotypes showed association with Rous sarcoma regression, but the Th-1 genotype did not. Chickens of the Ly-4a/Ly-4a, Bu-1b/Bu-1b and Ly-4b/Ly-4b, Bu-1a/Bu-1a genotypes had a significantly higher regressor ability than the other two double homozygous genotypes. These results indicate that higher regression is associated with (1) interaction between the Ly-4 and Bu-1 loci, and (2) complementation between either the line 6 Ly-4a allele and the line 100 Bu-1b allele, or the line 100 Ly-4b allele and the line 6 Bu-1a allele.

Animals↗
PubMed1986

Causes of mortality in chickens that regressed a Rous sarcoma virus-induced tumor.

Rous sarcomas were induced in 6-week-old chickens of several genetically different stocks: inbred lines C, 6(1), 6(3), and 7(2); crosses of inbred lines (6(3) X 7(2)) F4 and (6(1) X 15(1)) F2 X 6(1); and reciprocal crosses (15(1) X 100) F1 X 15(1) and (15(1) X 100) F1 X 100. The resulting tumors were scored for size six times during a 10-week period. Females that had completely regressed their sarcomas were placed in individual laying cages and examined weekly for reappearance of a tumor. After death, the probable cause was determined by necropsy. The major causes of death in the pooled sample of 49 females were fatty liver hemorrhagic syndrome (24.6%), reproductive disorder (14.2%), Marek's disease (12.2%), and lymphoid leukosis (6.1%). Elapsed time between tumor regression and death from any cause ranged from 21 days to 1930 days (5.3 years). One tumor recurred, this in a bird which eventually died with a massive sarcoma in the left wingweb and Rous metastasis in liver tissue. These data provide evidence of specific resistance to neoplastic disease.

Animals↗
PubMed1986

Metastasis of Rous sarcoma tumors in chickens is influenced by the major histocompatibility (B) complex and sex.

Six-week-old second generation progeny from the cross of inbred Lines 6(1) and 15(1), segregating into three major histocompatibility (B) complex groups (B2/B2, B2/B5, and B5/B5), were inoculated subcutaneously in the wingweb with one of three pseudotypes of Rous sarcoma virus. Chickens that died during a 10-week period after inoculation were necropsied and scrutinized for gross metastasis and histological sections of at least one lesion per affected organ examined for Rous sarcoma-transformed cells. By definition, a metastatic tumor was one located in an organ or tissue other than the primary inoculation site and having the histological appearance of a Rous sarcoma. Sarcomas developed in 1144 chickens, 390 of which died with tumor. For B2/B2, compared to B5/B5 hosts, mortality was 8 vs. 93%, median days to death were 45 vs. 31, and metastatic frequency was significantly lower, 32 vs. 58%. Disseminated lesions were significantly less frequent in females than males and grew preferentially in the heart and pericardial sac. Because the frequency of metastasis was significantly lower in B2/B2 than in B5/B5 chickens, a gene(s) within, or closely linked to, the B complex sharply retards the spread of Rous sarcoma virus-induced tumors.

Animals↗
PubMed1985

Major histocompatibility (B) complex effects on acquired immunity to cecal coccidiosis.

The influence of the major histocompatibility (B) complex on acquired immunity to the avian coccidium Eimeria tenella was studied in 217 F4 segregants (B2B2, B2B5, B5B5) of a cross between inbred lines 6(1) (B2B2) and 15(1) (B5B5) and segregating haplotype combinations of UNH105 (B23B23, B23B24, B24B24), a noninbred line of New Hampshire chickens. Chickens were immunized at 6 weeks of age with 500 oocysts daily for 5 days, then challenged 14 days later with 10 000 oocysts. Responses to infection were evaluated by cecal lesion scores, body weight gain, delayed wattle reaction (DWR), and spleen weight. The F4 segregants of genotypes B2B5 and B5B5 exhibited greater immunity to challenge than B2B2 chickens. B5B5 chickens showed a significantly greater DWR following immunization and larger spleens 6 days after the challenge than either of the other genotypes. However, both B2B5 and B5B5 chickens demonstrated significantly lower lesion scores than B2B2 chickens. There were no significant differences in weight gain among these genotypes. Among 139 line UNH105 segregants, B23B23 hosts had significantly lower lesion scores than B24B24 chickens. No other differences in immune response among line UNH105 genotypes were detected.

Animals↗
PubMed1985

MHC and non-MHC genetic influences on Rous sarcoma metastasis in chickens.

The B5/B5 genotype, in Leghorns, was associated with a high degree of metastasis of Rous sarcoma virus-induced tumors, but in combination with a Leghorn-New Hampshire background markedly less metastasis occurred. Initially, four mating types were used: B5/B5 X B5/B5 chickens from the F5 generation of the cross of Leghorn lines 6(1) and 15(1), B24/B24 X B24/B24 chickens from line UNH 105 (New Hampshires), and reciprocal crosses of B5/B5 X B24/B24 chickens. Subsequently, F2 generation progeny of the cross of B5/B5 and B24/B24 breeders, as well as B24/B24 line UNH 105 and B5/B5 (6(1) X 15(1))F2 chickens, were used. Six-week-old chickens were inoculated in the wingweb with Rous sarcoma virus. Chickens dying during a 10-week period after inoculation were necropsied and suspect metastatic lesions examined histologically. Among 234 terminal chickens from the initial four mating types the incidence of metastasis associated with B5/B5 Leghorns (66%) was substantially higher than for B24/B24 New Hampshires (12%) and B5/B24 progeny of reciprocal Leghorn-New Hampshire crosses (19 and 24%). Subsequently, among 524 terminal hosts in the Leghorn-New Hampshire F2 population, B genotype significantly influenced tumor dissemination. However, among 52 concurrently challenged B5/B5 hosts from the (6(1) X 15(1))F2 population the incidence of metastasis (60%) was significantly higher than among 122 B5/B5 hosts from the Leghorn-New Hampshire F2 population (31%), indicating a non-major histocompatibility complex genetic effect on metastasis.

Animals↗
PubMed1985

Estimates of heritability of response to Rous sarcomas of chickens.

The stocks used for this investigation consisted of 1039 F3 generation progeny from the cross of two highly inbred lines and 355 and 462 offspring from subpopulations UNH 105A and UNH 105B, respectively, of a noninbred line of New Hampshires. Matings were such that B complex alleles were segregated in the three experimental populations with minor exceptions. Each chicken was inoculated at 6 weeks of age with a subgroup of Rous sarcoma virus (RSV). Resulting tumors were subjectively scored on a scale from 0 (no tumor) to 6 (massive tumor) six times during a 10-week experimental period. Based upon the six tumor scores, each chicken was then assigned a tumor profile index (TPI), a criterion of antitumor response. The TPI were analyzed by least squares analysis of variance and corrected for hatch, sex, and virus prior to obtaining components of variance and estimates of heritability from a nested analysis of variance. Estimates of heritability from the sire component ranged from 0 to .41 +/- .27 and from the dam component .18 +/- .09 to .26 +/- .14, which are rather low estimates in general.

Animals↗
PubMed1985

Response of B complex haplotypes B22, B24, and B26 to Rous sarcomas.

Five individual male matings of line UNH 105 New Hampshires, in which all males and most females were either B22/B24 or B22/B26, produced 462 progeny that fell into six B complex genotypes: B22/B22, B24/B24, B26/B26, B22/B24, B22/B26, and B24/B26. The genotypes of parents and offspring were determined by blood typing for B alloantigens using a panel of antisera. Six-week-old chickens were inoculated with Rous sarcoma virus (RSV). Resulting tumors were scored for size six times over a 10-week period; based upon these scores, a tumor profile index (TPI) was assigned to each chicken as a criterion of immunological response. The B22/B26 hosts showed the greatest mean response (TPI 3.3) and B24/B24 chickens the lowest response (TPI 4.4), the difference being statistically significant. Dominance in the response to sarcoma was observed when either the B22 or B26 haplotype combined with the B24 haplotype and compared with the appropriate corresponding homozygotes, and when the B22 or B26 heterozygote was compared with B22/B22 and B26/B26 homozygotes.

Animals↗
PubMed1984

Solvent abuse associated pulmonary abnormalities.

Organic solvent inhalation leading to intoxication has become an important medical problem. Pulmonary function studies were performed on 42 young (ages 11-31) solvent inhalers and on 20 controls (ages 10-26). Ventilatory studies were normal in the majority, but residual volumes of inhalers were significantly higher (136.26% +/- 32.64% S.C.) than in controls (104% +/- 27.78% S.C.)--p less than 0.001. Lung tissue obtained at autopsy, from three known solvent inhalers was found to contain microscopic abnormalities similar to those seen in experimental panlobular emphysema and it is assumed these changes are consistent with increased residual volumes.

Adolescent↗
PubMed1983

Influence of non-MHC T lymphocyte alloantigens on regression of Rous sarcomas in the chicken.

Chickens of Regional Poultry Research Laboratory (RPRL) inbred line 6(3) regress sarcomas induced by Bryan high-titer Rous sarcoma virus to a greater extent than chickens of line 7(2), although these lines are identical for the major histocompatibility complex (MHC, B complex). They differ, however, at two independent autosomal loci, Ly-4 and Th-1, which determine surface alloantigens of partly overlapping subsets of T lymphocytes. Association of genotypes at these loci with quantitative variation in ability to regress Rous sarcomas was tested in segregating progeny derived from crosses of lines 6(3) and 7(2). In the F4 generation chickens of the Ly-4a/Ly-4a, Th-1a/Th-1a genotype (symbolized aa/aa) had significantly higher regressor ability than any of the other three double homozygous genotypes. In F5, all nine genotypes formed by combinations of homozygotes and heterozygotes were tested, and higher regressor ability was shown by the aa/aa, ab/aa, and aa/ab genotypes. These results indicate that higher regression is associated with: (1) interaction between the line 6(3) Ly-4a and Th-1a alleles in homozygous form; and (2) dominance x dominance interaction, in that the a allele at each locus is dominant for higher regression only within the homozygous aa genotype at the other locus.

Animals↗
PubMed1982

Complementation of major histocompatibility haplotypes in regression of Rous sarcoma virus-induced tumors in noninbred chickens.

Relative responses to Rous sarcoma virus (RSV)-induced tumors were studied in UNH 105 chickens, a noninbred line of New Hampshires. A total of 799 chickens blood typed for B alloantigens were classified into six genotypes: B23/B23, B24/B24, B26/B26, B23/B24, B23/B26, and B24/B26. Chickens were inoculated with subgroup A Rous sarcoma virus in the left wingweb at 6 weeks of age. The in vivo response was evaluated and given a tumor profile index (TPI) based on the change in tumor size over a 10-week period postinoculation. The TPI's ranged from 1 (regressor) to 3 (progressor). The mean TPI of B23/B26 hosts (1.7) was significantly smaller than that of all other genotypes studied. The mean TPI's of the homozygous genotypes B23/B23, B26/B26, and B24/B24, were 2.0, 2.3, and 2.9, respectively, and differed significantly in all comparisons. These results suggest complementation of haplotypes influencing the anti-Rous sarcoma response.

Animals↗
PubMed1982

Major histocompatibility complex (B): effect on the response of chickens to a second challenge with rous sarcoma virus.

The influence of B genotype on the formation of a second RSV-induced tumor was studied. Line 6(3) (B2/B2) and (6(1) x 15(1))F3 and F4 B2/B2 and B5/B5 chickens were challenged with RSV in the left wingweb at 6 weeks of age. Tumor-bearing animals then were rechallenged with RSV in the right wingweb at either 10, 11, or 12 days post primary inoculation. Most B2/B2 hosts resisted development of a second tumor compared to none of the B5/B5 hosts. Failure of a second tumor to develop in B2/B2 hosts was not explained by humoral neutralization of RSV in vivo, since sera from 83% of B2/B2 and 100% of B5/B5 tumor bearing chickens failed to neutralize virus prior to 12 days post primary inoculation. Humoral antiviral immunity appeared later in B5/B5 than in B2/B2 hosts. Humoral antiviral immunity appears to play little if any role in resistance to early RSV-induced tumor development, but likely both humoral and cell-mediated antitumor immunity do.

Animals↗
PubMed1981

Cross-reactivity between RSV-induced tumor antigen and B5 MHC alloantigen in the chicken.

Lymphocytes from chickens homozygous (B2B2) at the major histocompatibility complex (MHC) were tested for cytotoxic against five types of target chicken embryo fibroblasts (CEF). Lymphocytes from B2B2 chickens bearing RSV-induced tumors lysed in vitro targets of B2B2 and B5B5 RSV-infected CEF and B5B5 normal CEF, but did not lyse B2B2 and B24B24 normal CEF. Lymphocytes from normal B2B2 chickens did not lyse any of the five types of CEF targets. Alloantisera absorption studies showed that both RSV-infected and uninfected CEF shared alloantigens, in particular B-F alloantigens, with syngeneic erythrocytes. Absorption with B2B2 RSV-infected CEF significantly lowered the titer of B2B2 anti-B5B5 alloantisera. Cross-reactivity between B5 antigen(s) and tumor-associated antigen was suggested and the nature of the cross-reactivity was discussed. It is hypothesized that this cross-reactivity prevents B5B5 chickens from recognizing the RSV-induced tumors as foreign, enhances tumor growth and leads to death of the host.

Animals↗
PubMed1981

Increased growth of RSV-induced tumors in chickens partially tolerant to MHC alloantigens.

Chickens with B2B2 MHC genotypes were made partically tolerant to B5 MHC cell-surface antigens and the fate of their Rous-sarcoma-virus (RSV)-induced tumors was determined. B2B2 chickens partially tolerant to viable or lysed white blood cells (WBC) or viable red blood cells (RBC) from B5B5 chickens had a significantly higher incidence of tumor progression than untreated, PBS-treated, or B2B2 chickens inoculated with WBC from other B2B2 chickens. The criteria for tolerance were absence of antibody titer to the cell type inoculated and acceptance of allografts from B5B5 donors by B2B2 chickens. Graft-vs-host reactions occurred only in B2B2 chickens inoculated with viable WBC from B5B5 chickens. It appears that B2B2 chickens partially tolerant to B5 antigens failed to mount a successful immune response to RSV-induced tumors partly because of a B5 MHC antigen(s) cross-reacted with a tumor associated antigen(s) thereby severely limiting B2B2 host recognition of the tumor as foreign. Since WBC and RBC cell-surface antigens appear to contribute similarly to the effect, the B-F- region of the MHC may be involved.

Animals↗