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J Forman

Publications and source records attributed to J Forman.

At least 55 records · Page 3Linked to original sources
PubMed1988

Recognition by cytotoxic T lymphocytes of Qa-2 antigens. Sensitivity of Qa-2 molecules to phosphatidylinositol-specific phospholipase C.

Con A splenic lymphoblasts were incubated with phosphatidyl-inositol specific phospholipase C (PIPLC) derived from Bacillus thuringiensis and subsequently analyzed for Qa-2 Ag with the Qa-2 reactive mAb Qa-m2. This treatment completely removed Qa-2 detectable Ag on lymphoblasts from H-2d animals, indicating that these molecules are likely anchored to the cell membrane through phosphatidyl inositol (PI). Although exposure of lymphoblasts from H-2b mice to PIPLC greatly reduced Qa-2 expression, a subpopulation of cells retained a limited quantity of the Ag. Bulk cultured anti-Qa-2 CTL generated against the Qa-2 region from H-2b haplotype mice lysed Qa-2+ targets from B6.K2 (H-2b) and BALB/cJ (H-2d) animals. Pretreatment of these lymphoblast targets with PIPLC completely abolished lysis of the BALB/cJ target cells, whereas lysis of B6 targets was reduced only slightly. Anti-Qa-2 CTL clones tested against PIPLC-treated B6 target cells revealed two patterns of reactivity. One group of clones was unaffected in its ability to lyse PIPLC-pretreated targets and cross-reacted on Q6d/Ld molecules expressed on transfected L cells. A second group was unable to lyse PIPLC-pretreated lymphoblasts and cross-reacted on Q7d/Ld targets. These data suggest that H-2b-derived lymphoblasts express two different types of Qa-2 molecules with respect to PIPLC sensitivity; one type is sensitive to PIPLC and cross-reactive with Q7d, the other type is resistant to PIPLC and cross-reactive with Q6d. In contrast, H-2d lymphoblasts express only the PIPLC-sensitive type of molecules. It was also noted that bulk cultured anti-Qa-2 CTL more readily lysed H-2b target cells expressing a smaller quantity of PIPLC-resistant Ag than H-2d targets expressing a larger amount of PIPLC-sensitive Ag. Further, anti-Qa-2 CTL clones readily lysed PIPLC-treated target cells expressing very low levels of serologically detectable Qa-2. This suggests that recognition of class I molecules anchored to the membrane via a PIPLC-resistant linkage may more readily activate CTL for expression of lytic activity than molecules anchored through PI.

Animals↗
PubMed1988

An immunodominant epitope present in multiple class I MHC molecules and recognized by cytotoxic T lymphocytes.

CTL derived from (C3H x B6.K1)F1 animals were sensitized against L cells that express the transfected gene product Q10d/Ld. These CTL were highly crossreactive against three other class I molecules, H-2Kbm1, H-2Ld, and H-2Kd. In an attempt to define this crossreactive epitope it was noted that between 25 and 39% of amino acids in the alpha helices and central beta strands of these three molecules vary from Q10d. These amino acids represent residues that have been proposed to potentially interact with a peptide antigen or TCR (21). However, all four molecules share the amino acid tyrosine at positions 155 and 156. Additionally, Q10d, H-2Kbm1, and H-2Ld share alanine at position 152, while H-2Kd has an aspartic acid. We showed that these residues were important in controlling this epitope by the finding that anti-Q10d CTL did not recognize H-2Kbm1 revertant molecules that had either the position 152 alanine changed back to the wild-type H-2Kb residue (glutamic acid) or position 155 and 156 tyrosines changed back to wild-type residues arginine and leucine. Further evidence that these molecules share a crossreactive epitope was noted by the failure of (C3H x H-2Kbm1)F1 animals to generate CTL that recognized H-2Ld or H-2Kd, and the inability of (C3H x BALB/c)F1 animals to generate CTL reactive against H-2Kbm1. CTL from these mice were still able to recognize Q10d/Ld indicating that other epitopes could be detected if natural tolerance prevented recognition of the crossreactive epitope. To further define the epitope, CTL clones were generated against Q10d/Ld and maintained on either H-2Kbm1 or BALB/c feeder cells. In addition to testing these clones on the target cells described above, mutant molecules derived from H-2Ld, which have amino acid substitutions in their alpha 1 domain, were analyzed. It was noted that some anti-Q10 clones that did not crossreact on H-2Ld did react against H-2Ld mutant antigens that had H-2Dd amino acid substitutions in the alpha 1 domain at positions 63, 65, 66, and 70. Other clones had differential reactivities on these H-2Ld mutants further substantiating that alpha 1 domain amino acids play a role in controlling the expression of the crossreactive epitope. Thus, four class I molecules with multiple amino acid differences in their alpha 1 and alpha 2 domains share a crossreactive epitope readily recognized by alloreactive CTL.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1988

Selective expression of the Ly-6C.2 epitope on Lyt-2+ T cells that can develop in the absence of thymic influence.

The present study focused on attempts to correlate the expression of T cell differentiation antigens and development. A series of mAb was developed that recognized an Ly-6.2-linked Ag, Ly-6C.2. These mAb reacted with a subset of peripheral Lyt-2+ T lymphocytes but not Lyt-2+ thymocytes. Functional analysis of the Lyt-2+, Ly-6C.2- and Lyt-2+, Ly-6C.2+ subsets demonstrated that both cell types responded in class I and class II allogeneic MLC as well as in virus-specific cell-mediated cytolysis assay, although precursor frequency analysis suggested that the majority of precursor CTL were Ly-6C.2+. The marker did not appear to represent an activation Ag because Ly-6C.2-, Lyt-2+ precursor CTL generated Ly-6C.2-, Lyt-2+ CTL. Finally, virtually all splenic Lyt-2+ T cells from athymic (nu/nu) mice were Ly-6C.2+ whereas all thymic CTL were Ly-6C.2-. These results suggested that Ly-6C.2+, Lyt-2+ T cells may represent a distinct lineage of Lyt-2+ T cells that can develop in the absence of thymic influence.

Animals↗
PubMed1988

A third class I major histocompatibility complex antigen encoded by a gene in the D region of the H-2d haplotype recognized by cytotoxic T lymphocytes.

The D region of the H-2d haplotype contains five class I genes: H-2Dd, D2d, D3d, D4d and H-2Ld. Although previous studies have suggested the presence of D-end encoded class I molecules in addition to H-2Dd and H-2Ld, segregation of genes encoding such molecules has not been demonstrated. In this report we have used cytotoxic T lymphocytes (CTL) to examine the D region of the H-2d haplotype for the presence of additional class I molecules. CTL generated in (C3H x B6.K1)F1 (KkDk, KbDb) mice against the hybrid class I gene product Q10d/Ld expressed on L cells cross-react with H-2Ld but not H-2Dd molecules, as determined by lysis of transfected cells expressing H-2Ld but not H-2Dd. Although H-2Ld-specific monoclonal antibodies (mAb) completely inhibit H-2Ld-specific CTL from killing B10.A(3R) (KbDdLd) target cells, only partial inhibition of anti-Q10 CTL-mediated lysis was observed, suggesting the presence of an additional D-end molecule as a target for these latter CTL. To identify the region containing the gene encoding the Q10 cross-reactive molecule, we show that anti-Q10 CTL lyse target cells from a D-region recombinant strain B10.RQDB, which has H-2Dd, D2d, D3d, D4d, and H-2Db but not the H-2Ld H-2d, and H-2Ld (including D2d, D3d, and D4d), lacks this anti-Q10 CTL target molecule. Together, these data demonstrate that a class I gene mapping between H-2Dd and H-2Ld encodes an antigen recognized by anti-Q10 CTL. A likely candidate for this gene is D2d, D3d, or D4d.

Animals↗
PubMed1988

Linked recognition of helper and cytotoxic antigenic determinants for the generation of cytotoxic T lymphocytes.

These studies present a model for T-T collaboration for the generation of cytotoxic T lymphocytes. The in vitro CTL response against Qa-1 alloantigens in B6 Qa-1 congenic mice requires that animals are first primed in vivo with Qa-1 together with a second (helper) antigen. Both the antigen recognized by CTL (Qa-1) and Th (H-Y) must be presented on the same APC for successful priming. This findings is consistent with a linked recognition model whereby both molecules are presented on the same APC in order to accomplish close proximity between the two T cells. To further test this model, we demonstrated that in the absence of the helper antigen, H-Y, mice could be successfully primed against Qa-1 if coinoculated with a product of a Th, IL-2. We further showed that mice treated with anti-L3T4 antibodies could not be primed to Qa-1 even though the cells used for immunization expressed the H-Y helper antigen. Taken together, these results lend further support to a model of linked recognition between Th and CTL.P where close proximity allows for the lymphokine IL-2 to bind to its receptor on the CTL allowing for the successful induction of CTL.P.

Animals↗
PubMed1988

[Recurrent myocardial abscess during Streptococcus B endocarditis].

The authors report a case of serious streptococcus B endocarditis with a myocardial abscess that recurred after surgery. Streptococcus B endocarditis is a rare disease which is characterized by a pronounced tropism of the organism for cardiac tissues, with severe cardiac valve mutilation and abscess formation in 40% of the cases. A myocardial abscess makes the prognosis worse and must be treated surgically during the acute phase of endocarditis. Modern imaging methods, notably trans-oesophageal two-dimensional echocardiography and computerized tomography should now be used to detect such abscesses.

Abscess↗
PubMed1988

Left ventricular outflow obstruction after mitral valve repair (Carpentier's technique). Proposed mechanisms of disease.

Left ventricular outflow tract obstruction (LVOTO) after mitral valve repair by Carpentier's technique has been recently reported in the literature. To assess the mechanisms of this phenomenon, we investigated 307 mitral valve repairs performed between July 1985 and December 1986. Incidence of LVOTO related to the mechanism of the mitral insufficiency and to the etiology demonstrates a direct relation to preoperative mitral valve prolapse (posterior leaflet +/- anterior leaflet) of degenerative origin. No LVOTO occurred after rheumatic mitral insufficiency repair regardless of size of the left heart cavities or of the prosthetic ring. Intraoperative and surficial two-dimensional echocardiography, color Doppler methods, and cardiac catheterization were used to investigate the mechanisms leading to LVOTO. Nonspecific modifications induced by reduction in size of the mitral annulus by the prosthetic ring (anterior displacement of the posterior ventricular wall and of the posterior mitral leaflet and narrowing of the mitroaortic angle) are not sufficient to explain the LVOTO. The association of mitral leaflets (composed of excess tissue and opposed to flow by a perpendicular position attributable to a narrow mitroaortic angle) and geometric left ventricular modifications (responsible for the superposition of mitral inflow to ventricular outflow) also qualifies as a mechanism for the induction of LVOTO after mitral surgical repair.

Cardiac Catheterization↗
PubMed1987

Introduction of H-2Dd determinants into the H-2Ld antigen by site-directed mutagenesis.

We used site-directed mutagenesis to localize serologically defined (s) and CTL (c)-defined alloantigenic determinants to discrete amino acid sequences of a murine MHC class I antigen. Based on the prediction that amino acid position 63-73 of the H-2Dd antigen forms s-allodeterminants, the H-2Ld gene was mutated in a sequential fashion to replace codons for amino acid positions 63, 65, 66, 70, and 73 with those of the H-2Dd amino acids. Epitopes of the mutant antigens expressed in L-cells were examined by the binding of a series of mAbs specific for the H-2Dd antigen. The mutant antigen M66 had substitutions at residues 63, 65, and 66, and resulted in the acquisition of a number of H-2Dd-specific s-epitopes. Mutant M70 had an additional substitution at residue 70, which led to the gain of multiple additional H-2Dd s-epitopes. Together, more than half of all the relevant H-2Dd s-epitopes were mapped into amino acid position 63-70 of the H-2Dd molecule, which was expressed in the mutant H-2Ld gene. The final mutation at residue 73 (M73) caused no new epitope gains, rather, a few Dd s-epitopes acquired by the preceding mutations were lost. All of the H-2Ld-specific s-determinants were retained in the mutant molecules, as were H-2Dd s-determinants specific for the alpha-2 or alpha-3 domains. Changes of these residues affected c-determinants defined by CTL. Anti-H-2Dd CTL cultures and an anti-H-2Dd CTL clone recognized the mutant H-2Ld molecules, M66 and M70. Some CTL clones generated against the Q10d molecule, which has an identical sequence to H-2Dd between residues 61 and 73, failed to recognize native H-2Dd or Ld but did crossreact with mutant Ld. While bulk-cultured anti-H-2Ld CTL cultures reacted strongly against M73, bulk-cultured H-2Ld restricted anti-vesicular stomatitis virus CTL did not. Finally, at the clonal level two of three anti-H-2Ld CTL clones lost reactivity with some or all of these mutant molecules. From these results we conclude that a stretch of amino acids from position 63 to 70 of the alpha-1 domain controls major s- and c-antigenic sites on the H-2Dd antigen and c-sites on H-2Ld antigen.

Amino Acid Sequence↗
PubMed1987

Cytotoxic T lymphocytes from mice with soluble class I Q10 molecules in their serum are not tolerant to membrane-bound Q10.

Q10 is a class I Qa-2 region-encoded molecule that is secreted by the liver and present in serum at high concentrations (about 10 to 60 micrograms/ml) in most strains of mice. The amino terminal portion of this molecule can also be expressed as an integral membrane protein by splicing the 5' end of the Q10 gene to the 3' end of H-2Ld and transfecting the hybrid gene into murine L cells. Because CTL primarily recognize polymorphic determinants controlled by the alpha 1 and alpha 2 domains of class I molecules and because the Q10d/Ld product expressed by transfected L cells includes the alpha 1 and alpha 2 domains of Q10d, we could address whether mice bearing serum Q10 were tolerant to this molecule at the CTL level. The results of these experiments demonstrate that Q10+ mice are able to generate H-2-unrestricted CTL activity against Q10d expressed on transfected L cells, and this response was not inhibitable by the addition of Q10-containing normal mouse serum. It is unlikely that this CTL activity is due to possible polymorphic differences in Q10 alleles, since semisyngeneic BALB/c (H-2d) mice, from which the Q10d hybrid gene construct was derived, are able to generate anti-Q10d effector cells. The Q10d molecule was shown to cross-react with H-2Ld, lending support to the concept that Qa genes can serve as donors for polymorphic sequences found in H-2K, -D, and -L. That mice can generate anti-Q10 CTL activity suggests that this soluble class I protein does not act as a toleragen for these cells. The implications of these findings for an understanding of self-tolerance are discussed.

Animals↗
PubMed1987

Quantification of aortic regurgitation using Doppler imaging.

Aortic insufficiency induces the development of a jet within the left ventricular outflow tract. The cross sectional area of this jet at its origin is the major determinant of the severity of the regurgitation. M mode Doppler imaging reportedly allows the measurement of jet diameter. This study was designed to evaluate the quantification of aortic regurgitation using a measurement of the jet diameter by M mode Doppler imaging. The left ventricular outflow tract of 32 patients was imaged using either a multigate pulsed Doppler velocimeter of color flow mapping system (Hewlett Packard). The jet diameter was compared to a 4 grade semiquantification derived from supravalvular aortography. Adequate imaging was obtained in the 32 patients. Four of them had no regurgitation: no diastolic flow image could be found during their Doppler investigation. A clear jet image was obtained in the 28 remaining patients. We found a close relationship between the jet diameter (jd in mm) and the angiographic grade (ag): jd = 2.4 + 6.1 ag, r = 0.88, the most significant differences being found between grade 0 and grade 1, and grade 1 and grade 2. In conclusion, direct M mode measurement of the regurgitant jet of aortic insufficiency at its origin offers an additional approach of the severity of the leak.

Adult↗
PubMed1987

Doppler imaging of regurgitant jet in aortic insufficiency: experimental validation and preliminary clinical evaluation.

Aortic insufficiency induces the development of a jet within the left ventricular outflow tract. The diameter of a laminar jet is a well-defined hydraulic parameter. This study was designed to evaluate, both experimentally and in patients, the accuracy of its measurement using a Doppler imaging performed with a multigate pulsed Doppler velocimeter. The experimental validation was conducted on a water tank pulsatile model including calibrated orifices. Jet images appeared clearly delineated and were not modified when changing imaging angulation (from 85 degrees to 65 degrees), pump frequency (from 60 to 100 c min-1), pump output (from 0.5 to 3.8 l min-1), wall filtering, orifice shape, or signal-to-noise ratio. The measured jet diameter (jd) correlated closely with the orifice diameter (od): jd (mm) = 1.22 + (0.79 X od), r = 0.98. A preliminary clinical evaluation was performed on jets of aortic insufficiency on a series of 26 patients. Jet cross-section was studied within the left ventricular outflow tract using a parasternal approach. A high setting of wall filters allowed good quality imaging in 24 patients. In the absence of a diastolic jet, jd was taken equal to 0. Measured jet diameters were compared to the angiographic grade (ag): jd (mm) = 2.7 + (3.9 X ag), r = 0.86. In conclusion, jet diameter measurement using M-mode Doppler imaging is experimentally accurate and potentially valuable in patients with aortic insufficiency.

Aortic Valve Insufficiency↗
PubMed1987

[Foreign body in the tricuspid valve with valvular insufficiency and right-left shunt].

We present the case of a 50-year old man who progressively developed tricuspid valve insufficiency with opening of a patent foramen ovale responsible for right-to-left shunt with polycythaemia. The tricuspid valve insufficiency was due to a foreign body, probably of surgical origin as suggested by its radiological image and by the patient's previous history. It would have been introduced, far away from the tricuspid valve (compound fracture of the wrist), several years previously. At surgery, we found the foreign body embedded in the valve system. As a possible mechanism for the mutilation, an undiagnosed endocarditis was suspected but could not be confirmed. Three cases tricuspid endocarditis (with foreign bodies in the right ventricle) and 3 cases of asymptomatic tricuspid valve foreign bodies have been published. Fifty-five cases of foreign bodies introduced peripherally and migrated into the heart, the pericardium and the pulmonary artery are reviewed.

Coronary Circulation↗
PubMed1987

Detection of serum antibody response to Bacteroides bivius by enzyme-linked immunosorbent assay in women with intraamniotic infection.

Amniotic fluid from patients with intraamniotic infection usually reveals multiple organisms, including aerobes, anaerobes, and mycoplasmas. Bacteroides bivius, one of the most common isolates in these fluids, is found in approximately 20% of cases. To provide further information of the role of B bivius in intraamniotic infection, we measured serum immunoglobulin G (IgG) against B bivius by a micro-enzyme linked immunosorbent assay. Antigen was prepared from whole cells of a clinical isolate. Amniotic fluid was collected by aspiration of a transcervical pressure catheter, and was cultured for aerobes, anaerobes, and mycoplasmas. Acute and convalescent sera from 47 infected women and 31 controls were assayed to detect serologic response. Patients with intraamniotic infection and B bivius in amniotic fluid culture had significantly greater serologic responses than did infected women without B bivius in amniotic fluid and asymptomatic controls. These data suggest a pathogenic role of B bivius in intraamniotic infection, and imply that it probably plays a frequent role in other obstetric infections.

Adult↗
PubMed1986

Analysis of hybrid H-2D and L antigens with reciprocally mismatched aminoterminal domains: functional T cell recognition requires preservation of fine structural determinants.

Studies of immune recognition of hybrid class I antigens expressed on transfected cells have revealed an apparent general requirement that the N(alpha 1) and C1(alpha 2) domains be derived from the same gene in order to preserve recognition by virus-specific H-2-restricted and allospecific T cells. One exception has been the hybrid DL antigen in which the N domain of H-2Ld has been replaced by that of H-2Dd. Cells bearing this molecule serve as targets for some virus and allospecific CTL. Because cells expressing the reciprocal hybrid LD (N domain of H-2Dd replaced by that of H-2Ld) antigen have not been available, it has not been possible to evaluate whether this exception stemmed from the relatedness of H-2Ld and H-2Dd or whether the DL antigen fortuitously preserved some function of the parent molecule as a rare exception. To assess this question, and to evaluate the contribution of the N and C1 domains of H-2Ld and H-2Dd to serologic and T cell recognition, we have constructed the reciprocal chimeric gene pLD (the N exon of H-2Ld substituted for that of H-2Dd), introduced this into mouse L cells by DNA-mediated gene transfer, and analyzed the expressed product biochemically, serologically, and functionally. Transformant L cells expressing either LD or DL antigens were both reactive with a number of anti-H-2Ld or anti-H-2Dd N/C1-specific monoclonal antibodies, indicating the preservation in the hybrid molecules of determinants controlled by discrete domains. Mab binding was generally greater with cells expressing hybrid DL antigen than with those transformants expressing LD molecules. Moreover, the amount of beta 2M associated with DL antigens was more than that associated with LD. Cells expressing hybrid DL antigens were recognized as targets by bulk and cloned allospecific anti-H-2Dd and anti-H-2Ld CTL, whereas cells expressing LD molecules were not recognized by any of the T cells tested. VSV-specific H-2Ld-restricted CTL failed to lyse VSV-infected targets expressing either DL or LD. These results indicate that T cell reactivity of cells expressing the DL hybrid antigen is an exception to the observed general requirement for class I antigens to possess matched N and C1 domains for functional T cell recognition by T cells restricted to parental antigens.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acid Sequence↗
PubMed1986

Structure and function of three novel MHC class I antigens derived from a C3H ultraviolet-induced fibrosarcoma.

The UV-induced, C3H fibrosarcoma, 1591, expresses at least three unique MHC class I antigens not found on normal C3H tissue. Here we report the complete DNA sequence of the three novel class I genes encoding these molecules, and describe in detail the recognition of the individual products by tumor-reactive and allospecific CTL. Remarkably, although C3H does not appear to express H-2L locus information, this C3H tumor expresses two distinct antigens, termed A149 and A166, which are extremely homologous to each other and to the H-2Ld antigen from BALB/c. The gene encoding the third novel class I antigen from 1591, A216, is quite homologous to H-2Kk) throughout its 3' end. Since all three of these genes account for polymorphic restriction fragments not found in C3H, it is likely that they were derived by recombination from the endogenous class I genes of C3H. The DNA sequence homology of A149, A166, and H-2Ld is especially significant given the functional conservation observed between the products of these genes. Limited sequence substitutions appear to correlate with some of the discrete serological differences observed between these molecules. In addition, both A149 and A166 crossreact, but to differing extents, with H-2Ld at the level of T cell recognition. Our results are consistent with the view that CTL recognize complex conformational determinants on class I molecules, but extend previous observations by comparing a set of antigens with discrete and overlapping structural and functional differences.

Animals↗
PubMed1986

Growth inhibition of a B cell leukemia: evidence implicating an anti-idiotype immune response for protective tumor immunity.

BCL1, a spontaneous surface IgM (mu lambda)-positive (sIgM+) B cell leukemia of BALB/c (Igha) origin rarely grows in the Ig heavy chain (Igh) congenic mouse C.B-20 (Ighb) but is highly metastatic and lethal in the host strain of origin. Previous studies indicated that BCL1 tumor immunity in C.B-20 mice was associated with a T cell-mediated immune response against H-40, a minor histocompatibility (H) antigen controlled by a gene linked to the Igh locus. However, we observed that BCL1 leukemia grew progressively in BAB-14 (Igha/b) mice, a strain capable of generating an anti-H-40 immune response. This suggested that anti-H-40 immunity was insufficient for protection and implied that an Igh-V (variable) region gene product was also important for BCL1 growth inhibition. We therefore evaluated the role of two possible Igh-V region-linked gene products in BCL1 growth inhibition; namely, an Igh-V region-linked minor H antigen or alternatively the BCL1 IgM idiotype (Id). We could find no evidence for an Igh-V region-linked minor H antigen because immunosuppressed (500 R) CB-20 mice reconstituted with C.B-20 anti-BAB-14 splenocytes were susceptible to BCL1 growth, whereas recipients reconstituted with C.B-20 anti-BALB/c splenocytes were resistant to BCL1 challenge. In contrast, C.B-20 mice immunized against purified BCL1 IgM protein could adoptively confer BCL1 tumor immunity. C.B-20 mice immunized against other BALB/c IgM myeloma proteins containing either lambda or kappa light chains failed to protect C.B-20 mice suggesting that recognition of a unique determinant (Id) and not an allotype was crucial for tumor immunity. The BCL1 mu-chain appeared to make the major contribution to the idiotypic determinant because a hybridoma product composed of BCL1 mu-chains and BALB/c kappa-chains still elicited BCL1 immunity. Adoptive transfer of C.B-20 anti-BCL1 Id splenocytes into irradiated recipients that prevented an anti-H-40 response due to H-40 tissue expression failed to adoptively confer BCL1 immunity. Thus, these data suggest that BCL1 growth inhibition requires a T cell-mediated response against both H-40 and the BCL1 Id; these responses must be elicited concurrently in the tumor-bearing host to achieve protective BCL1 immunity.

Animals↗