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PubMed1988

Transfer of specific immunity in marrow recipients given HLA-mismatched, T cell-depleted, or HLA-identical marrow grafts.

The transfer of tetanus toxoid (TT) and diphtheria toxoid (DT) specific immunity was evaluated in 209 short-term (less than 120 days postgrafting) and 257 long-term (greater than 198 days postgrafting) non-boosted recipients after HLA-identical, HLA non-identical, and HLA-identical T cell-depleted marrow transplantation. TT or DT immunizations were not given to donors in the 6 months prior to transplant and the recipients received no immunizations post-transplantation. In 209 short-term recipients, 94% and 74% of recipients had detectable anti-TT and anti-DT titers respectively. In long-term recipients, 110 of 210 (52%) who received HLA-identical grafts, 17 of 38 (45%) who received HLA-non-identical grafts, and seven of seven (100%) who received HLA-identical T cell-depleted grafts had anti-TT titers; and 86 of 212 (40%) who received HLA-identical grafts, 11 of 38 (29%) who received HLA-non-identical grafts, and four of seven (57%) who received HLA-identical T cell-depleted grafts had anti-DT titers. When compared to non-boosted normal donor and control subjects, the magnitudes of anti-TT and anti-DT titers from the recipients were comparable to controls. These data show that transferred specific immunity is detectable in long-term recipients of T cell-depleted or HLA-non-identical grafts without immunizations of donors or recipients before or after transplantation.

Antibodies↗
PubMed1984

Facb rosette-forming cells in mice: studies on their functional significance.

Lymphocytes bearing receptors for the Facb fragment of IgG have been shown previously to be elevated in the peripheral blood of patients with rheumatoid arthritis. The generation of these cells and their possible functional role in immune regulation have been investigated in mice. Facb rosette-forming (Facb-R+) lymphocytes were found to be elevated in the spleens of mice mounting a secondary plaque-forming cell (PFC) response to sheep erythrocytes but not during the primary response. Splenic Facb-R+ lymphocytes were also elevated when a cross-reacting antigen (goat erythrocytes) was used for the secondary immunization but not when a non-cross-reacting antigen (chicken erythrocytes) was used. Both primary and secondary immunization with bacterial lipopolysaccharide resulted in elevation of splenic Facb-R+ lymphocytes. Administration of antigen-specific Facb fragment in conjunction with antigen (calf erythrocytes) produced a suppression of the secondary PFC response. However, F(ab')2 fragments produced no such effect. This suppressive effect was shown to be antigen-specific since administration of Facb fragment of anti-calf erythrocyte IgG had no suppressive effect on the secondary PFC response to sheep erythrocytes. No change in splenic Facb-R+ lymphocytes was observed during delayed hypersensitivity responses to either sheep erythrocytes or the contact-sensitizing agent oxazolone. These results indicate that Facb-R+ lymphocytes are generated during secondary humoral responses but not cell-mediated immune responses, and suggest that these cells may exert a suppressive influence on antibody production. These findings are discussed in relation to the occurrence of these cells in patients with rheumatoid arthritis.

Animals↗
PubMed1999

Naïve cytotoxic T lymphocytes spontaneously acquire effector function in lymphocytopenic recipients: A pitfall for T cell memory studies?

Whether memory T cells require persisting antigen for their survival has been a matter of debate. One prominent view that memory T cells do not require persisting antigen is based in part on studies in which T cell populations have been transferred into antigen-free mice. To generate "space" recipients were often irradiated; the functional properties of the transfused T cells were then evaluated after prolonged periods. In this report we show that transferring cytotoxic T lymphocytes (CTL) into irradiated or T and B cell-deficient hosts results in their proliferation and a change of their activation state. Moreover, naïve T cell receptor-transgenic CTL specific for the lymphocytic choriomeningitis virus glycoprotein spontaneously developed cytotoxic effector function under such conditions. Therefore, some of the conclusions based on transfer of T cell populations into irradiated recipients to investigate T cell memory may have to be reevaluated.

Adoptive Transfer↗
PubMed1999

Different stimulating effects of complement C3b and complete Freund's adjuvant on antibody response.

Upon activation, complement C3 undergoes a conformational change and acquires the capacity to covalently bind to other proteins such as antigen and to interact with specific receptors; therefore, C3 is involved in cell mediated immune response. The adjuvant effect produced by linking C3-fragments to antigen has recently been described. We injected C3b-Ag complexes consisting of one molecule of C3b ester linked to one molecule of HEL to immunised mice, and we compared the C3b adjuvant activity with that of complete Freund's adjuvant. IgG titers elicited by HEL emulsified in CFA (HEL + CFA) were higher than those elicited by HEL-C3b, but decreased rapidly after a peak response around day 45 whereas HEL-C3b resulted in a continuous increase of anti-HEL response. Mice immunised with HEL + CFA then boosted with HEL-C3b gave significantly higher response than those boosted with HEL + CFA, indicating more efficient memory cell restimulation by C3b. HEL + CFA leads to better priming than HEL-C3b when mice are boosted with HEL-C3b. Thus, adjuvant effect of C3b is different from that of CFA, leading to more stable IgG production and better memory stimulation.

Adjuvants, Immunologic↗
PubMed1996

CD8 T cell memory in B cell-deficient mice.

Antigen presentation by B cells and persistence of antigen-antibody complexes on follicular dendritic cells (FDC) have been implicated in sustaining T cell memory. In this study we have examined the role of B cells and antibody in the generation and maintenance of CD8+ cytotoxic T lymphocyte (CTL) memory. To address this issue we compared CTL responses to lymphocytic choriomeningitis virus (LCMV) in normal (+/+) versus B cell-deficient mice. The CTL response to acute LCMV infection can be broken down into three distinct phases: (a) the initial phase (days 3-8 after infection) of antigen-driven expansion of virus-specific CD8+ T cells and the development of effector CTL (i.e., direct ex vivo killers); (b) a phase of death (between days 10 and 30 after infection) during which >95% of the virus-specific CTL die and the direct effector activity subsides; and (c) the phase of long-term memory (after day 30) that is characterized by a stable pool of memory CTL that persist for the life span of the animal. The role of B cells in each of these three phases of the CTL response was analyzed. We found that B cells were not required for the expansion and activation of virus-specific CTL. The kinetics and magnitude of the effector CTL response, as measured by direct killing of infected targets by ex vivo isolated splenocytes, was identical in B cell-deficient and +/+ mice. Also, the expansion of CD8+ T cells was not affected by the absence of B cells and/or antibody; in both groups of mice there was an approximately 10,000-fold increase in the number of LCMV-specific CTL and a greater than 10-fold increase in the total number of activated (CD44hi) CD8+ T cells during the first week after virus infection. Although no differences were seen during the "expansion" phase, we found that the "death" phase was more pronounced in B cell-deficient mice. However, this increased cell death was not selective for LCMV-specific CTL, and during this period the total number of CD8+ T cells also dropped substantially more in B cell-deficient mice. As a result of this, the absolute numbers of LCMV-specific CTL were lower in B cell-deficient mice but the frequencies were comparable in both groups of mice. More significantly, the memory phase of the CTL response was not affected by the absence of B cells and a stable number of LCMV-specific CTL persisted in B cell-deficient mice for up to 6 mo. Upon reinfection, B cell-deficient mice that had resolved an acute LCMV infection were able to make accelerated CTL responses in vivo and eliminated virus more efficiently than naive B cell-deficient mice. Thus, CTL memory, as assessed by frequency of virus-specific CTL or protective immunity, does not decline in the absence of B cells. Taken together, these results show that neither B cells nor antigen-antibody complexes are essential for the maintenance of CD8+ CTL memory.

Animals↗
PubMed2001

Immunogenicity of two peptide determinants in the cytolytic T-cell response to flavivirus infection: inverse correlation between peptide affinity for MHC class I and T-cell precursor frequency.

We used the CD8+ cytotoxic T (Tc) cell immune response against the flavivirus, Murray Valley encephalitis virus (MVE), restricted by the H-2Kk major histocompatibility complex (MHC) class I molecule, to investigate immunodominance. Split-clone limiting dilution analysis revealed almost exclusive recognition of two peptides, MVE1785 and MVE1971, derived from the viral NS3 protein. The precursor frequency of MVE-reactive Tc cells was determined by limiting dilution analysis for cytotoxic function and intracellular staining for interferon-gamma; the latter gave a 100-fold higher estimate of MVE-reactive Tc cell precursors. MHC class I cell surface stabilization assays revealed that affinity for H-2Kk as well as halflives of the peptide-H-2Kk-complexes were markedly different for the two peptides. However, a kinetic study of antigen presentation showed that both peptides are presented for recognition by Tc cells with a comparable kinetics during the latent period of virus infection. Nevertheless, the lower affinity peptide MVE1785 elicited roughly twofold more Tc cell clones than the high-affinity peptide MVE1971. While the cytolytic activity against both determinants was similar after in vitro restimulation at the peak of the primary response, the smaller pool of memory anti-MVE1971 Tc cells correlated with an impaired memory response against that determinant, suggesting that the available T-cell repertoire is a major factor influencing the establishment of T-cell memory.

Animals↗
PubMed1992

The lineage relationship between virgin and memory B cells.

J11d is expressed on a variety of hemopoietic cells, including B cells. In previous studies, we have shown that B cells are heterogeneous with respect to their levels of J11d expression and that memory B cells are contained within the J11dlo B cell population. In this report, we have further examined the relationship between memory precursors and memory cells. We have found that the ability of J11dlo B cells from unprimed mice to respond to primary antigenic stimulation was generally low; the lowest response occurred following immunization with soluble antigen in vitro. Following adoptive transfer into irradiated mice and repeated stimulation of these mice with antigen, J11dlo cells generated memory responses which were similar to those generated by J11dlo memory cells obtained from primed mice. In contrast, J11dhi B cells from unprimed mice gave rise to both primary and memory responses, but the memory responses were lower than those generated by J11dlo cells. Although the expression of J11d on both J11dhi and J11dlo cells from unprimed mice decreased after adoptive transfer, J11dlo, as compared to J11dhi, virgin cells proliferated more rapidly. These results suggest that memory responses are elaborated predominantly from J11dlo virgin cells. Taken together with previous results, our studies indicate that, J11dlo B cells are different from J11dhi B cells. Hence, they are either memory precursors or are memory cells.

Animals↗
PubMed1989

Studies on B-cell memory. IV. Effects of lipopolysaccharide on primary and secondary antibody responses to T-independent type-2 (TI-2) antigen in mice.

Effects of LPS on primary and secondary antibody responses to typical TI-2 antigens were investigated in mice. Simultaneous injection of LPS with a TI-2 antigen showed only little adjuvant effect on the following primary antibody response to the antigen. In contrast, either a single or multiple injections of LPS, prior to the immunization with a TI-2 antigen, significantly augmented the following primary antibody response to the antigen. LPS, however, inhibited the development of B-cell memory to a TI-2 antigen when administered together with the antigen. Moreover, an injection of LPS in mice, which had strong IgM and IgG B-cell memories to a TI-2 antigen, caused disappearance or profound reduction of the memories. The results suggest that LPS produced by gram-negative bacteria exerts inhibitory effects on the development and continuation of B-cell memory to bacterial infections.

Adjuvants, Immunologic↗
PubMed1997

Somatic mutation leads to efficient affinity maturation when centrocytes recycle back to centroblasts.

Although most mutations are deleterious, an interplay between somatic mutation and selection within germinal centers (GC) results in rapid generation of high affinity memory B cells. How high affinity B cells with large numbers of mutations are generated and preserved within GC containing at their peak only a few thousand cells has been puzzling. We have developed a model of somatic mutation and B cell expansion within a GC that resolves this puzzle. We show that the frequent recycling of Ag-selected centrocytes back into centroblasts can lead to efficient affinity maturation. Memory cells are generated in large numbers even when most of the selected centrocytes recycle back into centroblasts. Our model suggests that a germinal center reaction in which the output of cells is low up to the point of GC dissociation, followed by the release of centrocytes into the periphery, is advantageous for generating high affinity memory.

Animals↗
PubMed2003

Memory lanes.

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Animals↗