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Results for “Immunity, Humoral”

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PubMed1994

Coronary atherosclerosis in transplanted mouse hearts. II. Importance of humoral immunity.

Obstructive lesions in arterial vessels of transplanted organs constitute an important factor in the late failure of these organs, especially for the heart. The absence of obstructive lesions in syngeneic donor-recipient combinations, suggests that they depend upon recipient immune responsiveness. It is controversial whether humoral or cellular aspects of the immune response predominate in the process. The present experiments employed hearts transplanted between inbred mice. After brief preoperative immunosuppression of recipients with mAbs to CD4 and CD8 determinants, hearts transplanted between mice incompatible for histocompatibility Ags survived for prolonged periods and most developed typical, obstructive coronary lesions. Our quantitative scoring of vascular changes on tissue sections of excised hearts, grades both their severity and prevalence. Transplants between strains that produced Abs to donor cells (B10.A to B10.BR), developed coronary lesions exceeding those in the reverse combination in which no detectable Ab was formed (B10.BR to B10.A; p < 0.00001), even though their histoincompatibility was similar. Treatment of B10.A recipients of B10.BR hearts with an antiserum against the donor significantly increased coronary lesions (p < 0.0003) in a dose-dependent fashion. Coronary arteries of B10.BR hearts transplanted to C.B-17 SCID mice remained largely free of lesions, whereas transplants to SCID recipients that received continuing injections of an antiserum directed to Ags of the donor developed striking, obstructive coronary lesions. We conclude that humoral immunity can be the prime instigator of atheromatous changes that occur in transplanted hearts.

Animals↗

PubMed2001

Discordant cellular and humoral immune responses to cytomegalovirus infection in healthy blood donors: existence of a Th1-type dominant response.

Previous studies have documented discordant cellular and humoral immune responses to subjects exposed to HIV-1, and that the nature of such responses may determine susceptibility and resistance to disease. We determined whether there is a spectrum of cellular versus humoral immunodominant responses to cytomegalovirus (CMV) infection. Blood samples from 50 healthy blood donors were tested for anti-CMV IgG antibodies and for proliferative responses of peripheral blood mononuclear cells (PBMC) to CMV antigens. Four patterns of immune responses to CMV were found: no detectable response (30%, Ab(-)/Tc(-)), anti-CMV IgG only (28%, Ab(+)/Tc(-)), both anti-CMV IgG and T lymphocyte proliferation to CMV antigens (18%, Ab(+)/Tc(+)), and, interestingly, T lymphocyte proliferation to CMV only (24%, Ab(-)/Tc(+)). To determine whether these immunodominant phenotypes correlate with the ability of PBMC to secrete IL-2 and IFN-gamma in response to CMV antigens, we found that a greater percentage of individuals with a T cell proliferative response to CMV antigens (Ab(-)/Tc(+) and Ab(+)/Tc(+)) responded with increased IL-2 (P = 0.001) and IFN-gamma levels (P = 0.002), compared to those without a proliferative response (Ab(-)/Tc(-) and Ab(+)/Tc(-)). Our data therefore demonstrate that different individuals exhibit different immunodominant patterns of response to CMV. In particular, some individuals who are exposed to CMV fail to develop an antibody response but do develop cellular immunity. Whether these different patterns predict susceptibility or resistance to CMV-induced disease remains to be determined.

Adult↗

PubMed2001

Maturation of xenoantibody gene expression during the humoral immune response of rats to hamster xenografts.

Immunoglobulin isotype switching represents an important component of antibody maturation in the development of humoral immune responses. We have recently conducted a series of studies in a nonimmunosuppressed rodent model to define the kinetics of xenoantibody production and seek evidence for the maturation of xenoantibody Ig gene expression by xenograft recipients. LEW rats were transplanted with hamster cardiac xenografts and the grafts were allowed to remain in situ for prolonged immune stimulation of the host. Anti-hamster antibodies were examined at days 4, 8, 21, 28 and 40 post-transplantation. cDNA libraries specific for rat mu or gamma heavy chains were constructed from B lymphocytes of the xenograft recipients at day 4 and day 21 post-transplantation. Selected cDNA clones encoding the Ig V(H)HAR family of genes from each group were sequenced and analyzed for the presence of somatic mutations. We found that the reactivity of xenoantibodies examined with flow cytometry underwent sequential changes in which IgM titers peaked at day 8 post-transplantation (PTx) and returned to low levels after 21 days. IgG titers started to increase at about one week PTx and peaked at 21-28 days. All the IgG isotypes (IgG1, 2a, 2b and 2c) were differentially involved in the IgG responses. Serum passive transfer experiments demonstrated that IgM antibody fractions separated from sera at day 4 post-transplantation were capable of causing hyperacute rejection (HAR) of hamster xenografts, whereas IgM fractions from days 21-40 failed to cause HAR (N = 7, MST = 4 days), a pattern that was consistent with a rise in total xenoreactive IgM levels at days 4-8 and a fall to low levels at 21 days post-transplantation. IgG-containing fractions separated from day 21-40 antisera caused HAR (N = 7, MST = 36 min) whereas IgG fractions from day 8 sera failed to induce graft rejection. Genetic analysis of the rearranged VH genes from 10 cDNA clones demonstrated that the Ig mu (n = 5) and gamma (n = 5) chain clones used the same family of VH genes (V(H)HAR family) to encode their antibody binding activity. The majority (80%) of the IgM clones were present in their original germline configuration. In contrast, the nucleotide sequences from IgG clones manifested an increase in the numbers of replacement mutations in the CDR region of the Ig heavy chain genes, providing evidence for a potential role for somatic mutation in the maturation of IgG xenoantibody responses as the humoral response matures with time post-transplantation.

Amino Acid Sequence↗

PubMed1997

A Phase I clinical trial of immunotherapy with interferon-gamma gene-modified autologous melanoma cells: monitoring the humoral immune response.

BACKGROUND: Tumor cells transduced with cytokine genes provide immunogenic vaccines for cancer immunotherapy. METHODS: A Phase I clinical trial was conducted for the specific active immunization of melanoma patients with interferon-gamma (IFN-gamma) gene-modified autologous melanoma tumor cells. Short term melanoma cultures were transduced retrovirally with the gene for human IFN-gamma. The genetically modified melanoma cells secreted biologically active IFN-gamma and showed enhanced expression of major histocompatibility complex class I and class II surface antigens. These cells were inactivated by irradiation (50 gray) and were cryopreserved for the vaccine. Twenty melanoma patients were enrolled in this clinical trial. The immunizations were administered in escalating doses once every 2 weeks for 3 months. The first and second injections consisted of 2 million cells, followed by 6 million for the third and fourth injections, and then 18 million for the fifth and sixth injections. The humoral immune responses of the patients were assessed by enzyme-linked immunoadsorbent assay, radioimmunoassay, and radioimmunoprecipitation. RESULTS: Thirteen of the 20 patients completed the immunization protocol. Eight of these 13 patients showed a humoral immunoglobulin (Ig)G response against autologous and allogeneic melanoma cells. The other five patients either had no detectable antimelanoma antibodies or showed a weak IgG response that did not rise significantly above the preimmune level. All the sera contained low or undetectable levels of antimelanoma IgM antibodies. The IgG response increased progressively in titer during the course of immunization. The positive sera showed preferentially strong binding to melanoma cell lines and some cross-reactivity to nonmelanoma tumors. A 75-80 kD antigen on melanoma cells was immunoprecipitated by postimmune sera of 3 of the responding patients. Preimmune sera from these three patients and sera from other patients immunized with a standard nontransduced melanoma cell vaccine failed to precipitate this antigen. Two patients with significant increases in serum IgG had clinical tumor regression, and two additional patients with low serum IgG response had transient shrinkage of nodular disease during therapy. CONCLUSIONS: These data suggest that gene therapy with IFN-gamma-transduced melanoma cells is safe and worthy of further investigation in patients with less advanced stage malignant melanoma. The ability to monitor changes in the humoral responses of the immunized patients has been demonstrated.

Cancer Vaccines↗

PubMed1991

The effect of restraint stress on the kinetics, magnitude, and isotype of the humoral immune response to influenza virus infection.

The stress of physical restraint has been shown to modulate the cellular immune response during a viral infection. We have studied the effects of stress on the humoral immune response during infection by influenza virus. Restraint stress altered the kinetics of the antibody response; seroconversion in the IgG and IgA isotypes was delayed in virus-infected C57BL/6 mice subjected to repeated cycles of physical restraint. However, the magnitude and isotype of the mature antibody response were unaffected during the plateau phase; no significant differences were observed between restrained/infected and nonrestrained/infected mice. Thus, the time during infection at which the antibody response was measured was a significant variable in the study of stress-induced alterations of the host's response to a replicating viral antigen. While restraint stress did not significantly affect the magnitude or class of the humoral response, it did alter the kinetics of response.

Animals↗

PubMed2002

Bilamellar cationic liposomes protect adenovectors from preexisting humoral immune responses.

Adenoviral vectors have been widely used for gene therapy, but they are limited both by the presence of a humoral immune response that dramatically decreases the level of transduction after reinjection and by their requirement for target cells to express appropriate receptors such as Coxsackie adenovirus receptor (CAR). To overcome both limits, we encapsulated adenovectors using bilamellar DOTAP:chol liposomes. Electron micrography (EM) showed that these liposomes efficiently encapsulated the vectors, allowing CAR-independent adenovector transduction of otherwise resistant cells. DOTAP:chol-encapsulated adenovectors encoding LacZ or alpha(1)-antitrypsin inhibitor (AAT) were also functionally resistant ex vivo and in vivo to the neutralizing effects of human anti-adenoviral antibodies, unlike other liposomal systems. Hence, bilamellar DOTAP:chol liposomes may be useful for applications using adenovectors in which the target cells lack adenoviral receptors or in which the recipient already has or develops a neutralizing antibody response that would otherwise inactivate readministered vector.

Adenoviridae↗

PubMed1994

An early humoral immune response in peripheral blood following parenteral inactivated influenza vaccination.

The enzyme-linked immunospot assay was used to examine the humoral immune response in 15 healthy volunteers immunized with either split or subunit inactivated trivalent influenza vaccine containing A/Beijing/353/89 (H3N2), A/Taiwan/1/86 (H1N1) and B/Yamagata/16/88. The rapidity of the individual B-cell and serum antibody response was examined in lymphocyte and serum samples collected at various time intervals after vaccination. A rapid serological response was detected with increases in antibody titre detected in the majority of volunteers by 7-8 days postvaccination. Influenza-specific plasma cells were detected as early as 4 days postvaccination, higher numbers of IgA and IgG antibody-secreting cells (ASC) were observed which peaked at 7-8 days postvaccination. The number of ASCs then declined, with low numbers of cells detected at 11 days postvaccination. Influenza-specific IgA ASCs were predominantly of the IgA1 subclass. This rapid immune response may have a bearing on future vaccination policies of unimmunized 'at risk groups' in times of high influenza activity.

Adult↗

PubMed1991

Major reproduction hormones as regulators of cell-to-cell interactions in humoral immune responses.

The effects of chorionic gonadotropin (CG), estradiol, and progesterone on the cell mechanisms that determine the rate of the humoral immune response have been investigated in experiments on ovariectomized and noncastrated mice. CG (40 IU) injected into noncastrated animals increased the antibody response to sheep erythrocytes (SRBC), whereas a higher dose of the hormone (200 IU) had no effect. In contrast, both hormone doses inhibited the immune response in ovariectomized animals. Injection of estradiol (2.5 micrograms/day), but not progesterone (0.2 mg/day), into ovariectomized mice stimulated the immune response, indicating a possible role of estrogens as mediators of CG immuno-stimulating effect in noncastrated animals. Both CG does inhibited suppressor cell generation in noncastrated mice, whereas in ovariectomized animals, the hormonal effect was directly opposite. Sex steroid hormones did not influence the formation of suppressor cells. In a syngeneic transfer system, the hormones under study did not change the activity of helper T cell precursors. However, CG administration to noncastrated recipients stimulated an adoptive immune response in a dose-dependent manner. Estradiol, but not progesterone, has the same effect in ovariectomized mice. CG administration (200 IU) to ovariectomized recipients inhibited the plaque-forming cell response. This CG effect depended upon prostaglandin synthetase activity.

Animals↗

PubMed1999

Humoral immune parameters in Atlantic cod (Gadus morhua L.) I. The effects of environmental temperature.

The effects of environmental temperature on certain humoral immune parameters in Atlantic cod (Gadus morhua L.) were studied. Serum samples were collected from captive cod, of wild origin, kept at different temperatures for 12 months. It was found that immunoglobulin and natural antibody levels increased with increasing temperature whereas the total serum protein concentration, anti-protease activity, iron concentration, unsaturated and total iron binding capacity decreased with increasing temperature. Haemolytic activity and percentage iron saturation also tended to decrease with increasing temperature although this was not statistically significant.

Adaptation, Physiological↗

PubMed1982

Abnormal humoral immune responses in peripheral blood lymphocyte cultures of bone marrow transplant recipients.

The present study was aimed at investigating recovery of humoral immunity in vitro after bone marrow transplantation in patients with acute leukemia and severe aplastic anemia. Hemolytic plaque assays were utilized to quantitate pokeweed mitogen-stimulated polyclonal immunoglobulin production and sheep erythrocyte antigen-specific antibody responses in cultures of peripheral blood mononuclear cells of 39 patients beginning at 1 month, for variable periods up to a maximum of 4 years after marrow transplantation. Three phases were identified: an early period of primary B cell dysfunction with concomitant immunoregulatory T cell abnormalities--i.e., decreased helper and increased suppressor activities; an intermediate phase in which B cell dysfunction could be attributed in large measure to immunoregulatory T cell abnormalities; and a late phase of normal B and T lymphocyte functions. Patients with graft-versus-host disease differed from those without it in that they often did not manifest increased T cell suppressor activity in the early period, and they were noted to have prolonged and profound B and T cell abnormalities in the chronic phase of their disease. In selected patients, simultaneous assessment of ratios of Leu-2 to Leu-3 antigens on T cells by monoclonal antibodies and of immunoregulatory T cell functions revealed a correlation between the two only late in the post-transplant period. These studies provide an insight into the ontogeny of B cell function in the post-transplant period and indicate that in certain situations phenotypic alterations in T cell subsets cannot reliably be used to predict abnormalities in their function in recipients of marrow transplantation.

Acute Disease↗

PubMed1991

Humoral immune response against contractile proteins (actin and myosin) during cardiovascular disease.

Sensitive and highly specific ELISA assays were developed to determine humoral immune response against actin and myosin in 122 patients suffering from various cardiovascular diseases: acute viral myocarditis (n = 10, MYO), acute myocardial infarction (n = 28, AMI), valve surgery (n = 35, VALVE), coronary bypass surgery (n = 35, CABG), and peripheral vascular surgery (n = 14, VASC). Anti-actin and anti-myosin antibodies were determined on admission and serially during a period of 90 days. Anti-actin and anti-myosin immune response (IgG, IgM) was expressed comparing absorbance of the patients' serum with a reference serum. In the different patient groups significantly (P less than 0.01) higher anti-actin and anti-myosin antibody concentrations were found on admission compared with age-matched control groups. During follow-up, all patient groups except the vascular surgery group showed a significant immune response against actin and myosin, with an immune response ratio (peak/admission) for AMA IgG and IgM respectively of 2.12 and 2.40 in the VALVE group, 1.30 and 1.99 in the CABG group, 1.42 and 1.48 in the AMI group and 1.66 and 1.25 in the MYO group; and for AAA IgG and IgM respectively of 1.57 and 3.00 in the VALVE group, 1.54 and 1.64 in the CABG group, 1.25 and 1.07 in the AMI group, and 1.42 and 1.42 in the MYO group. A significant correlation between pre-cardiac injury and peak post-cardiac injury anti-myosin and anti-actin autoantibody levels could be demonstrated suggesting that pre-injury sensitization to these antigens plays an important role in evoking post-cardiac injury immune response.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗

PubMed1990

Humoral immunity of the oral cavity during remission-induction therapy in patients with acute myeloid leukaemia.

To evaluate whether local oral humoral immunity changes during remission-induction therapy of newly diagnosed acute myeloid leukaemia, 10 consecutive adult patients were investigated during 4 weeks. The concentrations of the oral secretory immunoglobulins A and M were increased during the first 7 days but, when corrected for changes in the salivary flow rate, the secretion rates of S-IgA and S-IgM remained unchanged, relative to the values before chemotherapy. In comparison, the concentrations of the serum immunoglobulins A, G and M were decreased, like the leukocyte and thrombocyte counts, during the first 14 d. It is concluded that the chemotherapeutic agents appear to act differently upon the local plasma cells associated with oral secretory glands and plasma cells in the bone marrow, and that the secretion rate of oral immunoglobulins remains constant during remission-induction therapy.

Adult↗

PubMed1980

Cell-mediated and humoral immunity to herpesviruses during and after herpes zoster infections.

The influence of herpes zoster virus infection on cell-mediated and humoral immunity to varicella-zoster virus (VZV), cytomegalovirus, and herpes simplex virus (HSV) was followed in 17 zoster patients from the first week to 6 months after start of eruptions. The clinical responses were registered and correlated to the immune responses. A significant depression in blast transformation on stimulation of lymphocytes with all three antigens was found on days 1 to 5 compared with transformations later after zoster eruptions and compared with controls. Phytohemagglutinin exhibited the same stimulation in the different groups and controls. No significant differences in interferon production in the various groups and controls were found on stimulation with the VZV and HSV antigens. All zoster patients became seropositive by complement fixation to VZV a few days after start of the zoster eruption. Two zoster patients showed a fourfold rise in complement fixation antibodies to HSV. Three patients had changes in complement fixation titers to cytomegalovirus, which could indicate new infection or reactivation of infection with this virus. A significant lower transformation index to VZV was found during the first 9 days in zoster patients with fever compared with patients without fever. The relevance of this observation is discussed in relation to a previous similar observation from our group.

Adult↗

PubMed2005

Multiclade human immunodeficiency virus type 1 envelope immunogens elicit broad cellular and humoral immunity in rhesus monkeys.

The development of a human immunodeficiency virus type 1 (HIV-1) vaccine that elicits potent cellular and humoral immune responses recognizing divergent strains of HIV-1 will be critical for combating the global AIDS epidemic. The present studies were initiated to examine the magnitude and breadth of envelope (Env)-specific T-lymphocyte and antibody responses generated by vaccines containing either a single or multiple genetically distant HIV-1 Env immunogens. Rhesus monkeys were immunized with DNA prime-recombinant adenovirus boost vaccines encoding a Gag-Pol-Nef polyprotein in combination with either a single Env or a mixture of clade-A, clade-B, and clade-C Envs. Monkeys receiving the multiclade Env immunization developed robust immune responses to all vaccine antigens and, importantly, a greater breadth of Env recognition than monkeys immunized with vaccines including a single Env immunogen. All groups of vaccinated monkeys demonstrated equivalent immune protection following challenge with the pathogenic simian-human immunodeficiency virus 89.6P. These data suggest that a multicomponent vaccine encoding Env proteins from multiple clades of HIV-1 can generate broad Env-specific T-lymphocyte and antibody responses without antigenic interference. This study demonstrates that it is possible to generate protective immune responses by vaccination with genetically diverse isolates of HIV-1.

AIDS Vaccines↗

PubMed1999

[Beta-endorphin involved in the regulation of humoral immune function of rats during acute hypoxia].

In order to investigate the role of beta-endorphin in the regulation of humoral immune function of rats during acute hypoxia, the effects of beta-endorphin on mitogen-induced spleen lymphocyte DNA synthesis and hemolysin formation as well as IgG production to chicken egg albumen were observed. It was found that after rats received icv injection of beta-endorphin (1 ng/rat), the T-lymphocyte DNA content, the hemolysin-forming capacity of SRBC-sensitized rats and the IgG level were reduced significantly compared with the control (icv normal saline). Similar suppressive effects on immune function could be found after rats were exposed to 7 km altitude in a hypobaric chamber for 48 h. Pretreatment with icv injection of naltrexone, the immunosuppressive effects of acute hypoxia were partially blocked. Icv administration of beta-endorphin produced an increase in splenic cathcholamines, similar to those of hypoxia treated group (7 km for 12 h). All the above findings suggest that beta-endorphin may modulate the immune response to hypoxia stress via opioid receptor and its inhibitory action may be mediated by activating sympathetic nervous system.

Adjuvants, Immunologic↗

PubMed2005

Humoral immune response against mycobacterial antigens in bronchoalveolar fluid from tuberculosis patients.

Resistance to tuberculosis (TB) is cell-mediated but a humoral response is common and may be correlated with the lack of effective local cellular defense mechanisms. The goal of the study was to evaluate IgG, IgA, and IgM-mediated humoral immune response against 38-kDa+16-kDa and 38-kDa+lipoarabinomannan (LAM) mycobacterial antigens in bronchoalveolar fluid (BALF) from patients with pulmonary TB. Non-tuberculosis (NTB) patients were used as control. 179 BALF samples (56 TB and 123 NTB) were examined. Commercially available ELISA-based assays against proteins 38-kDa and 16-kDa or 38-kDa plus LAM were used. Three different dilutions of BALF: 1:1; 1:10, and 1:50 (100) were tested. Only the results obtained with the 1:10 dilution allowed distinguishing TB and NTB groups. The mean IgG level for 38-Da+LAM was significantly higher in the TB than that in the NTB group (P<0.0001). The mean IgA level for 38-kDa+LAM also was higher in the TB group (P<0.05). No difference was observed between TB and NTB groups in the titer of IgM antibodies. These findings indicate that TB is associated with the presence of detectable levels of antibodies in BALF. The antibody response is highly heterogeneous. This phenomenon results from the balance between pathogen and host immune system. The tests examined for detection of IgG in BALF can be used in combination with other diagnostic methods to increase diagnostic accuracy of pulmonary TB.

Antibodies, Bacterial↗

PubMed1990

[Indices of humoral immunity in inhabitants of the Far North infected and sick with tuberculosis].

As a result of a complex study of the humoral immunity indices in tuberculosis infected and affected inhabitants of the Extreme North with reference to the immunoglobulin A, G, M levels, titers of heterohemagglutinins (HHA) and specific antibodies defined by means of indirect hemagglutination test (IHAT), complement fixation test with tuberculin and IHAT with phosphatidic antigen (IHAT-Ph), two simple and quite informative tests, i.e. HHA and IHAT-Ph, are recommended for the practical use in health system. HHA level greater than 1/4 indicates the absence of immunodeficiency in system B. The results of IHAT-Ph, being adequate to the main clinical manifestations of tuberculosis (including bacillary excretion and lung tissue destruction), can be used as an additional diagnostic and evaluation method of tuberculous activity when the subjects from specific infection foci are examined or during their inpatient and dispensary observation and management.

Adult↗

PubMed1989

Humoral immunity in allograft rejection. The role of cytotoxic alloantibody in hyperacute rejection and enhancement of rat cardiac allografts.

The role of humoral immunity in graft rejection in the rat model remains controversial. Passive transfer of cytotoxic alloantibody (CAA) has resulted either in hyperacute rejection or in graft enhancement. This study examines the effect of transfer of CAA on cardiac allograft survival in three rat strain combinations that are fully mismatched at the major histocompatibility (MHC) loci. Strain-specific immune responsiveness in donor-recipient pairs varied from low (Lewis-to-ACI) to high (ACI-to-Lewis) as measured by mixed lymphocyte reactions. CAA was obtained from rats sensitized by three successive skin grafts at weekly intervals. Group 1 (high responder recipients), which consisted of Lewis rats presensitized to ACI and had a lymphocytotoxicity titer of 1:512 to 1:2048, rejected ACI cardiac allografts in 10.8 +/- 7.2 hr compared with 6.5 +/- 0.5 days in naive controls (p less than 0.001). Injection of 1 ml of high-titer CAA into naive Lewis rats immediately after ACI cardiac grafting led to hyperacute rejection of ACI hears in 2.1 +/- 0.8 hr while 1 ml of CAA followed by 2 ml of guinea pig complement (GPC) resulted in even faster rejection (mean survival time (MST) of 23.8 +/- 4.7 min). Injection of 2 ml GPC alone or in combination with 1 ml naive Lewis serum had no effect on graft survival. Multiple pretransplant injections of 1 ml of CAA on days -3, -2,-1, and 0 relative to transplantation resulted in significant prolongation of allograft survival (MST of 10.3 +/- 0.3 days; P less than 0.01). In group 2 (intermediate responder recipients), where Lewis rats were presensitized to WF strain and where cytotoxicity titer was 1:16 to 1:256, the recipients rejected WF hearts in 23.8 +/- 5.8 hr compared with 6.8 +/- 0.8 days in unsensitized control recipients (P less than 0.001). Injection of 1 ml of Lewis anti-WF CAA resulted in prolonged graft survival of 9.7 +/- 3.5 days, while injection of 1 ml of CAA followed by 2 ml of GPC caused hyperacute rejection in 104 +/- 61.7 min. Pretransplant injections of CAA on days -3, -2, -1, and 0 resulted in enhancement, with an MST of 16.3 +/- 1.3 days (P less than 0.001). In group 3 (low responder recipients), ACI presensitized to Lewis developed a cytotoxicity titer of 1:2 to 1:32 and rejected Lewis hearts in 5.3 +/- 0.4 days compared with 10.6 +/- 1.0 days in naive recipients.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗