Induction of Antibody Responses In Vivo by Antigen Specific Helper Factor

ABSTRACT Gastric Helicobacter spp. induce chronic gastritis that may lead to ulceration and dysplasia. The host elicits a T helper 1 (Th1) response that is fundamental to the pathogenesis of these bacteria. We analyzed immune responses in Helicobacter-infected, normal mice depleted of CD4+ CD25+ T cells to investigate the in vivo role of regulatory T cells (Tregs) in the modulation of Helicobacter immunopathology. BALB/c and transgenic mice were depleted of CD4+ CD25+ T cells by administration of an anti-CD25 antibody either at the time of infection with Helicobacter or during chronic infection and gastritis. Depletion of CD25+ Tregs prior to and during infection of mice with Helicobacter spp. did not affect either bacterial colonization or severity of gastritis. Depletion of CD25+ Tregs was associated with increased Helicobacter-specific antibody levels and an altered isotype distribution. Paragastric lymph node cells from CD25+ Treg-depleted and control infected mice showed similar proliferation to Helicobacter antigens, but only cells from anti-CD25-treated animals secreted Th2 cytokines. CD25+ Tregs do not control the level of gastritis induced by gastric Helicobacter spp. in normal, thymus-intact BALB/c mice. However, CD25+ Tregs influence the cytokine and antibody responses induced by infection. Autoimmune gastritis is not induced in Helicobacter-infected mice depleted of CD25+ Tregs but is induced in CD25+ Treg-depleted mice, which have a higher frequency of autoreactive T cells.

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8-mercaptoguanosine-mediated enhancement of in vivo IgGl, IgG2 and IgG3 antibody responses to polysaccharide antigens in normal and xid mice

Immunopharmacology ◽

10.1016/0162-3109(89)90018-0 ◽

1989 ◽

Vol 18 (3) ◽

pp. 205-212 ◽

Cited By ~ 11

Author(s):

James J. Mond ◽

Kenneth Hunter ◽

James J. Kenny ◽

Fred Finkelman ◽

Kim Witherspoon

Keyword(s):

Antibody Responses ◽

Polysaccharide Antigens

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Equine allogeneic bone marrow-derived mesenchymal stromal cells elicit antibody responses in vivo

Stem Cell Research & Therapy ◽

10.1186/s13287-015-0053-x ◽

2015 ◽

Vol 6 (1) ◽

Cited By ~ 65

Author(s):

Lynn M Pezzanite ◽

Lisa A Fortier ◽

Douglas F Antczak ◽

Jennifer M Cassano ◽

Margaret M Brosnahan ◽

...

Keyword(s):

Bone Marrow ◽

Mesenchymal Stromal Cells ◽

Stromal Cells ◽

Allogeneic Bone Marrow ◽

Antibody Responses ◽

Allogeneic Bone

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In vivo analysis of replication and immunogenicity of proviral clones of human T-lymphotropic virus type 1 with selective envelope surface-unit mutations

Blood ◽

10.1182/blood-2005-03-1076 ◽

2005 ◽

Vol 106 (10) ◽

pp. 3602-3608 ◽

Cited By ~ 10

Author(s):

Lee R. Silverman ◽

Andrew J. Phipps ◽

Andy Montgomery ◽

Soledad Fernandez ◽

Tomonori Tsukahara ◽

...

Keyword(s):

T Cell ◽

Antibody Response ◽

Virus Type ◽

Antibody Responses ◽

Envelope Gene ◽

Cell Leukemia Virus Type ◽

Surface Unit ◽

Human T Cell

AbstractHuman T-cell leukemia virus type 1 (HTLV-1) is the causative agent of adult T-cell lymphoma/leukemia (ATL). The HTLV-1 envelope gene exhibits limited variability when examined from infected individuals, but has not been tested using infectious clones of the virus in animal models. In vitro assays indicate that HTLV-1 envelope (Env) Ser75Ile, Asn95Asp, and Asn195Asp surface unit (SU) mutants are able to replicate in and immortalize lymphocytes. Herein, we examined the effects of these Env mutants in rabbits inoculated with HTLV-1 immortalized ACH.75, ACH.95, or ACH.195 cell lines (expressing full-length molecular clones with the SU mutations) or the ACH.1 cell line (expressing wild-type SU). All rabbits became infected, and the fidelity of the mutations was maintained throughout the 8-week study. However, SU point mutations resulted in decreased antibody responses to viral group-associated antigen (Gag) and Env antigens. ACH.195 rabbits had a selective decreased antibody response to SU, and one ACH.195 rabbit had an antibody response to both HTLV-1 and HTLV-2 SUs. Some mutant inoculation groups had altered proviral loads. However, peripheral-blood mononuclear cell (PBMC) proviral loads did not correlate with antibody responses. Our data are the first to demonstrate that mutations in critical determinants of HTLV-1 Env SU altered antibody responses and proviral loads, but do not prevent viral replication in vivo.

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Interferon activation status underlies higher antibody response to viral antigens in patients with systemic lupus erythematosus receiving no or light treatment

Rheumatology ◽

10.1093/rheumatology/keaa611 ◽

2020 ◽

Author(s):

Albin Björk ◽

Rui Da Silva Rodrigues ◽

Elina Richardsdotter Andersson ◽

Jorge I Ramírez Sepúlveda ◽

Johannes Mofors ◽

...

Keyword(s):

Antibody Response ◽

Specific Antibody ◽

Lupus Erythematosus ◽

Serum Proteins ◽

Light Treatment ◽

Antibody Responses ◽

Type I ◽

Specific Antibody Response ◽

Viral Antigens

Abstract Objectives Infections have been proposed as an environmental risk factor for autoimmune disease. Responses to microbial antigens may be studied in vivo during vaccination. We therefore followed patients with SLE and controls during split-virion influenza vaccination to quantify antibody responses against viral antigens and associated cellular and proteome parameters. Methods Blood samples and clinical data were collected from female patients with SLE with no or HCQ and/or low-dose prednisolone treatment (n = 29) and age- and sex-matched healthy controls (n = 17). Vaccine-specific antibody titres were measured by ELISA and IFN-induced gene expression in monocytes by quantitative PCR. Serum proteins were measured by proximity extension assay and disease-associated symptoms were followed by questionnaires. Results The vaccine-specific antibody response was significantly higher in patients compared with controls and titres of IgG targeting the viral proteins were higher in patients than controls at both 1 and 3 months after immunization. Clinical disease symptoms and autoantibody titres remained unchanged throughout the study. Notably, a positive pre-vaccination mRNA-based IFN score was associated with a significantly higher vaccine-specific antibody response and with a broader profile of autoantibody specificities. Screening of serum protein biomarkers revealed higher levels of IFN-regulated proteins in patients compared with controls and that levels of such proteins correlated with the vaccine-specific IgG response, with C-C motif chemokine ligand 3 exhibiting the strongest association. Conclusion Augmented antibody responses to viral antigens develop in patients with SLE on no or light treatment and associate with markers of type I IFN system activation at the RNA and protein levels.

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Induction and Measurement of In Vivo Antibody Responses

Current Protocols in Immunology ◽

10.1002/0471142735.im07016s00 ◽

1991 ◽

Vol 00 (1) ◽

pp. 7.16.1-7.16.7

Author(s):

Renata J.M. Engler ◽

Carole C. Kurman ◽

David L. Nelson

Keyword(s):

Antibody Responses

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Neutrophils Are Required During Immunization With the Pneumococcal Conjugate Vaccine for Protective Antibody Responses and Host Defense Against Infection

The Journal of Infectious Diseases ◽

10.1093/infdis/jiaa242 ◽

2020 ◽

Vol 222 (8) ◽

pp. 1363-1370 ◽

Cited By ~ 1

Author(s):

Essi Y I Tchalla ◽

Manmeet Bhalla ◽

Elizabeth A Wohlfert ◽

Elsa N Bou Ghanem

Keyword(s):

Conjugate Vaccine ◽

Survival Rates ◽

Antibody Responses ◽

Host Protection ◽

Lethal Infection ◽

Neutrophil Depletion ◽

Opsonophagocytic Killing ◽

Full Protection

Abstract Neutrophils can shape adaptive immunity; however, their role in vaccine-induced protection against infections in vivo remains unclear. Here, we tested their role in the clinically relevant polysaccharide conjugate vaccine against Streptococcus pneumoniae (pneumococcus). We antibody depleted neutrophils during vaccination, allowed them to recover, and 4 weeks later challenged mice with pneumococci. We found that while isotype-treated vaccinated controls were protected against an otherwise lethal infection in naive mice, full protection was lost upon neutrophil depletion. Compared to vaccinated controls, neutrophil-depleted mice had higher lung bacterial burdens, increased incidence of bacteremia, and lower survival rates. Sera from neutrophil-depleted mice had less antipneumococcal IgG2c and IgG3, were less efficient at inducing opsonophagocytic killing of bacteria by neutrophils in vitro, and were worse at protecting naive mice against pneumococcal pneumonia. In summary, neutrophils are required during vaccination for optimal host protection, which has important implications for future vaccine design against pneumococci and other pathogens.

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Synthetic nanoparticle vaccines produced by layer-by-layer assembly of artificial biofilms induce potent protective T-cell and antibody responses in vivo

Vaccine ◽

10.1016/j.vaccine.2010.10.001 ◽

2011 ◽

Vol 29 (3) ◽

pp. 558-569 ◽

Cited By ~ 26

Author(s):

Thomas J. Powell ◽

Naveen Palath ◽

Mary E. DeRome ◽

Jie Tang ◽

Andrea Jacobs ◽

...

Keyword(s):

T Cell ◽

Antibody Responses ◽

Layer By Layer ◽

Layer By Layer Assembly ◽

Layer Assembly

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Enhancement of in vitro and in vivo antigen-specific antibody responses by interleukin 11.

Journal of Experimental Medicine ◽

10.1084/jem.175.1.211 ◽

1992 ◽

Vol 175 (1) ◽

pp. 211-216 ◽

Cited By ~ 75

Author(s):

T G Yin ◽

P Schendel ◽

Y C Yang

Keyword(s):

T Cells ◽

Antibody Titer ◽

Specific Antibody ◽

Antibody Responses ◽

Rabbit Serum ◽

Dependent Manner ◽

Dose Dependent ◽

Interleukin 11

The availability of large quantities of highly purified recombinant interleukin 11 (rhuIL-11) has allowed us to investigate the effects of rhuIL-11 on sheep red blood cell (SRBC)-specific antibody responses in the murine system. The results showed that rhuIL-11 was effective in enhancing the generation of mouse spleen SRBC-specific plaque-forming cells (PFC) in the in vitro cell culture system in a dose-dependent manner. These effects of rhuIL-11 were abrogated completely by the addition of anti-rhuIL-11 antibody, but not by the addition of preimmunized rabbit serum. Cell-depletion studies revealed that L3T4 (CD4)+ T cells, but not Lyt-2 (CD8)+ T cells, are required in the rhuIL-11-stimulated augmentation of SRBC-specific antibody responses. The effects of rhuIL-11 on the SRBC-specific antibody responses in vivo were also examined. RhuIL-11 administration to normal C3H/HeJ mice resulted in a dose-dependent increase in the number of spleen SRBC-specific PFC as well as serum SRBC-specific antibody titer in both the primary and secondary immune responses. In mice immunosuppressed by cyclophosphamide treatment, rhuIL-11 administration significantly augmented the number of spleen SRBC-specific PFC as well as serum SRBC-specific antibody titer when compared with the cyclophosphamide-treated mice without IL-11 treatment. These results demonstrated that IL-11 is a novel cytokine involved in modulating antigen-specific antibody responses in vitro as well as in vivo.

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Antibody Responses with Fc-Mediated Functions after Vaccination of HIV-Infected Subjects with Trivalent Influenza Vaccine

Journal of Virology ◽

10.1128/jvi.00285-16 ◽

2016 ◽

Vol 90 (12) ◽

pp. 5724-5734 ◽

Cited By ~ 39

Author(s):

Anne B. Kristensen ◽

William N. Lay ◽

Fernanda Ana-Sosa-Batiz ◽

Hillary A. Vanderven ◽

Vijaya Madhavi ◽

...

Keyword(s):

Influenza Vaccine ◽

Cell Activation ◽

Seasonal Influenza ◽

Nk Cell ◽

Antibody Responses ◽

Hiv Positive ◽

Binding Assays ◽

Positive Group ◽

Hiv Negative

ABSTRACTThis study seeks to assess the ability of seasonal trivalent inactivated influenza vaccine (TIV) to induce nonneutralizing antibodies (Abs) with Fc-mediated functions in HIV-uninfected and HIV-infected subjects. Functional influenza-specific Ab responses were studied in 30 HIV-negative and 27 HIV-positive subjects immunized against seasonal influenza. All 57 subjects received the 2015 TIV. Fc-mediated antihemagglutinin (anti-HA) Ab activity was measured in plasma before and 4 weeks after vaccination using Fc-receptor-binding assays, NK cell activation assays, and phagocytosis assays. At baseline, the HIV-positive group had detectable but reduced functional Ab responses to both vaccine and nonvaccine influenza antigens. TIV enhanced Fc-mediated Ab responses in both HIV-positive and HIV-negative groups. A larger rise was generally observed in the HIV-positive group, such that there was no difference in functional Ab responses between the two groups after vaccination. The 2015 TIV enhanced functional influenza-specific Ab responses in both HIV-negative and HIV-positive subjects to a range of influenza HA proteins. The increase in functional Ab responses in the HIV-positive group supports recommendations to immunize this at-risk group.IMPORTANCEInfection with HIV is associated with increasing disease severity following influenza infections, and annual influenza vaccinations are recommended for this target group. However, HIV-infected individuals respond relatively poorly to vaccination compared to healthy individuals, particularly if immunodeficient. There is therefore a need to increase our understanding of immunity to influenza in the context of underlying HIV infection. While antibodies can mediate direct virus neutralization, interactions with cellular Fc receptors may be important for anti-influenza immunityin vivoby facilitating antibody-dependent cellular cytotoxicity (ADCC) and/or antibody-dependent phagocytosis (ADP). The ability of seasonal influenza vaccines to induce antibody responses with potent Fc-mediated antiviral activity is currently unclear. Probing the ADCC and ADP responses to influenza vaccination has provided important new information in the quest to improve immunity to influenza.

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