爬行动物的体液免疫

爬行动物针对颗粒性和可溶性抗原,能够快速、有效的产生抗体。爬行动物血清中的抗体主要包括高分子量的免疫球蛋白（HMWIg）和不止一种的低分子量免疫球蛋白（LMWIg）,爬行动物中还有在亲代和子代间传递的免疫球蛋白Ig Y。目前爬行动物免疫球蛋白的纯化方法主要有：硫酸铵沉淀法、联合凝胶过滤层析和离子交换层析法、Protein A亲和层析法。研究爬行动物体液免疫对研究动物免疫的进化及对病原控制具有重要意义。     

Disruption of IL-21 Signaling Affects T Cell-B Cell Interactions and Abrogates Protective Humoral Immunity to Malaria

Interleukin-21 signaling is important for germinal center B-cell responses, isotype switching and generation of memory B cells. However, a role for IL-21 in antibody-mediated protection against pathogens has not been demonstrated. Here we show that IL-21 is produced by T follicular helper cells and co-expressed with IFN-γ during an erythrocytic-stage malaria infection of Plasmodium chabaudi in mice. Mice deficient either in IL-21 or the IL-21 receptor fail to resolve the chronic phase of P. chabaudi infection and P. yoelii infection resulting in sustained high parasitemias, and are not immune to re-infection. This is associated with abrogated P. chabaudi-specific IgG responses, including memory B cells. Mixed bone marrow chimeric mice, with T cells carrying a targeted disruption of the Il21 gene, or B cells with a targeted disruption of the Il21r gene, demonstrate that IL-21 from T cells signaling through the IL-21 receptor on B cells is necessary to control chronic P. chabaudi infection. Our data uncover a mechanism by which CD4+ T cells and B cells control parasitemia during chronic erythrocytic-stage malaria through a single gene, Il21, and demonstrate the importance of this cytokine in the control of pathogens by humoral immune responses. These data are highly pertinent for designing malaria vaccines requiring long-lasting protective B-cell responses.     

Cell Interactions in Humoral and Cell-mediated Immunity

THYMUS-derived lymphocytes (T-cells) play an important role in the initiation of both humoral and cell-mediated immunity^1–3. We have investigated whether the helper function and the cell-mediated killer function of lymphocyte populations are performed by the same cells, by assaying thymus-derived lymphocytes both for their capacity to cooperate in vitro with bone marrow-derived lymphocytes (B-cells) in the induction of plaque-forming cells and for their capacity to cause in vitro complement independent lysis of target cells.     

Starvation Reveals Maintenance Cost of Humoral Immunity

Susceptibility to pathogens and genetic variation in disease resistance is assumed to persist in nature because of the high costs of immunity. Within immunity there are different kinds of costs. Costs of immunological deployment, the costs of mounting an immune response, are measured as a change in fitness following immunological challenge. Maintenance costs of immunity are associated with investments of resources into the infrastructure of an immune system and keeping the system at a given level of readiness in the absence of infection. To demonstrate the costs of immunological maintenance in the absence of infection is considered more difficult. In the present study we examined the maintenance costs of the immune system in lines of Drosophila melanogaster that differed in their antibacterial innate immune response under starved and non-starved conditions. Immunodeficient mutant flies that have to invest less in the immunological maintenance were found to live longer under starvation than wild type flies, whereas the opposite was found when food was provided ad libitum. Our study provides evidence for the physiological cost of immunological maintenance and highlights the importance of environmental variation in the study of evolutionary trade-offs.     

大豆低聚糖对小鼠体液免疫功能的影响试验研究

通过利用大豆低聚糖对小鼠灌服后溶血素生成量的测定,阐明大豆低聚糖对小鼠体液免疫功能的影响。     

Humoral and Cellular Immunity in Chromium Picolinate-Supplemented Lambs

The effects of oral supplementation of chromium picolinate (CrPic) on humoral and cellular immunity in sheep were investigated. Twenty-four male lambs divided into four treatments and received different dosages of CrPic: placebo (0), 0.250, 0.375, and 0.500 mg of chromium/animal/day during 84 days. The base ration was Panicum maximum cv Massai hay and concentrate. Blood samples were collected fortnightly for total and differential leukocyte counts. On days 28 and 56, the lambs were challenged with chicken ovalbumin I.M. Serum samples were collected on days 46 and 74 and subjected to an indirect enzyme-linked immunosorbent assay to measure IgG anti-ovalbumin. The cell-mediated immune response was determined by a delay-type hypersensitivity test using phytohemagglutinin. CrPic did not significantly affect humoral immunity in lambs but there was a negative effect on cellular immunity (P?<?0.05) as Cr supplementation increased. Therefore, the level of Cr supplementation for lambs must be better studied to address its effect on stressed animals or the possible toxic effects of Cr on the animal itself or its immune system.     

Behavioral Immunity Suppresses an Epizootic in Caribbean Spiny Lobsters

Sociality has evolved in a wide range of animal taxa but infectious diseases spread rapidly in populations of aggregated individuals, potentially negating the advantages of their social interactions. To disengage from the coevolutionary struggle with pathogens, some hosts have evolved various forms of “behavioral immunity”; yet, the effectiveness of such behaviors in controlling epizootics in the wild is untested. Here we show how one form of behavioral immunity (i.e., the aversion of diseased conspecifics) practiced by Caribbean spiny lobsters (Panulirus argus) when subject to the socially transmitted PaV1 virus, appears to have prevented an epizootic over a large seascape. We capitalized on a "natural experiment" in which a die-off of sponges in the Florida Keys (USA) resulted in a loss of shelters for juvenile lobsters over a ~2500km² region. Lobsters were thus concentrated in the few remaining shelters, presumably increasing their exposure to the contagious virus. Despite this spatial reorganization of the population, viral prevalence in lobsters remained unchanged after the sponge die-off and for years thereafter. A field experiment in which we introduced either a healthy or PaV1-infected lobster into lobster aggregations in natural dens confirmed that spiny lobsters practice behavioral immunity. Healthy lobsters vacated dens occupied by PaV1-infected lobsters despite the scarcity of alternative shelters and the higher risk of predation they faced when searching for a new den. Simulations from a spatially-explicit, individual-based model confirmed our empirical results, demonstrating the efficacy of behavioral immunity in preventing epizootics in this system.     

Type I Interferons Suppress Anti-parasitic Immunity and Can Be Targeted to Improve Treatment of Visceral Leishmaniasis

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Stearoyl-CoA Desaturase-Mediated Monounsaturated Fatty Acid Availability Supports Humoral Immunity

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Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection

Lyme Disease caused by infection with Borrelia burgdorferi is an emerging infectious disease and already by far the most common vector-borne disease in the U.S. Similar to many other infections, infection with B. burgdorferi results in strong antibody response induction, which can be used clinically as a diagnostic measure of prior exposure. However, clinical studies have shown a sometimes-precipitous decline of such antibodies shortly following antibiotic treatment, revealing a potential deficit in the host’s ability to induce and/or maintain long-term protective antibodies. This is further supported by reports of frequent repeat infections with B. burgdorferi in endemic areas. The mechanisms underlying such a lack of long-term humoral immunity, however, remain unknown. We show here that B. burgdorferi infected mice show a similar rapid disappearance of Borrelia-specific antibodies after infection and subsequent antibiotic treatment. This failure was associated with development of only short-lived germinal centers, micro-anatomical locations from which long-lived immunity originates. These showed structural abnormalities and failed to induce memory B cells and long-lived plasma cells for months after the infection, rendering the mice susceptible to reinfection with the same strain of B. burgdorferi. The inability to induce long-lived immune responses was not due to the particular nature of the immunogenic antigens of B. burgdorferi, as antibodies to both T-dependent and T-independent Borrelia antigens lacked longevity and B cell memory induction. Furthermore, influenza immunization administered at the time of Borrelia infection also failed to induce robust antibody responses, dramatically reducing the protective antiviral capacity of the humoral response. Collectively, these studies show that B. burgdorferi-infection results in targeted and temporary immunosuppression of the host and bring new insight into the mechanisms underlying the failure to develop long-term immunity to this emerging disease threat.     

Humoral Immunity Links Candida albicans Infection and Celiac Disease

Objective

The protein Hwp1, expressed on the pathogenic phase of Candida albicans, presents sequence analogy with the gluten protein gliadin and is also a substrate for transglutaminase. This had led to the suggestion that C. albicans infection (CI) may be a triggering factor for Celiac disease (CeD) onset. We investigated cross-immune reactivity between CeD and CI.

Methods

Serum IgG levels against recombinant Hwp1 and serological markers of CeD were measured in 87 CeD patients, 41 CI patients, and 98 healthy controls (HC). IgA and IgG were also measured in 20 individuals from each of these groups using microchips sensitized with 38 peptides designed from the N-terminal of Hwp1.

Results

CI and CeD patients had higher levels of anti-Hwp1 (p=0.0005 and p=0.004) and anti-gliadin (p=0.002 and p=0.0009) antibodies than HC but there was no significant difference between CeD and CI patients. CeD and CI patients had higher levels of anti-transglutaminase IgA than HC (p=0.0001 and p=0.0039). During CI, the increase in anti-Hwp1 paralleled the increase in anti-gliadin antibodies. Microchip analysis showed that CeD patients were more reactive against some Hwp1 peptides than CI patients, and that some deamidated peptides were more reactive than their native analogs. Binding of IgG from CeD patients to Hwp1 peptides was inhibited by γIII gliadin peptides.

Conclusions

Humoral cross-reactivity between Hwp1 and gliadin was observed during CeD and CI. Increased reactivity to Hwp1 deamidated peptide suggests that transglutaminase is involved in this interplay. These results support the hypothesis that CI may trigger CeD onset in genetically-susceptible individuals.     

Cellular and Humoral Immunity: a Distinction in Antigenic Recognition

THERE is little or no humoral cross reactivity between the native and denatured forms of a protein antigen. Antibodies to native bovine ribonuclease do not bind ribonuclease oxidized with performic acid^1–3, indicating that antibodies can distinguish between two molecular conformations. There is no humoral cross reactivity between rabbit IgG and the product of reduction of all the disulphide bridges^4–6. Also there is essentially no serological cross reactivity between lysozyme and its reduced and S-carboxymethylated (CM-lysozyme) derivative^7–9.