Development of monoclonal antibodies (MAbs) to feline interferon (fIFN)-<i>γ</i> as tools to evaluate cellular immune responses to feline infectious peritonitis virus (FIPV)

Satoh, Ryoichi; Kaku, Ayumi; Satomura, Megumi; Kohori, Michiyo; Noura, K.; Furukawa, Tomoko; Kotake, Masako; Takano, Tomomi; Hohdatsu, Tsutomu

doi:10.1016/j.jfms.2011.01.008

Cited by 11 publications

(18 citation statements)

References 40 publications

(27 reference statements)

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“…Based on the above findings, it was suggested that memory CD4 + and CD8 + T cells, i.e., the cellular immune response, may participate in viral clearance in recovered SARS patients. We similarly showed that peripheral blood mononuclear cells (PBMCs) obtained from FIPVinfected non-FIP cats specifically and significantly produced feline IFN-␥ (fIFN-␥) against heat-inactivated FIPV stimulation, while those from FIP cats did not [19,20]. These results support the previous finding that T helper (Th)1 activity plays an important role in defense against FIPV infection.…”

Section: Introductionsupporting

confidence: 87%

“…PBMCs were prepared as described by Satoh et al [19]. fIFN-␥ was measured by sandwich ELISA, as described previously [20], to evaluate Th1 immune activity in PBMCs. PBMCs (5 × 10 6 cells/ml) were cultured with each synthesized peptide (30 g/ml), heat-inactivated virus (FIPV KU-2 strain, 10 4.6 TCID 50 /ml; FIPV 79-1146 strain, 10 5.0 TCID 50 /ml) as a positive control, or culture medium alone as a negative control at 37 • C for 9 days.…”

Section: Sandwich Elisa To Detect Fifn-in Pbmcs Culture Supernatantsmentioning

confidence: 99%

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Screening and identification of T helper 1 and linear immunodominant antibody-binding epitopes in spike 1 domain and membrane protein of feline infectious peritonitis virus

Takano

Morioka

Gomi

et al. 2014

Vaccine

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Feline infectious peritonitis virus (FIP virus: FIPV) causes a fatal disease in wild and domestic cats. The development of an FIP-preventive vaccine requires an antigen that does not induce antibody-dependent enhancement, and T helper (Th)1 activity plays an important role in protect against FIPV infection. In the present study, we identified synthetic peptides including Th1 and a linear immunodominant antibody-binding epitope in the S1 domain and M protein of FIPV. We also identified peptides that strongly induce Th1 activity from those derived from the structural proteins (S, M, and N proteins) of FIPV based on this and previous studies (Satoh et al. [19]). No Th1 epitope-containing peptide was identified in the peptides derived from the S1 domain of type I FIPV. In contrast, 7 Th1 epitope-containing peptides were identified in the S1 domain of type II FIPV, and no linear immunodominant antibody-binding epitope was contained in any of these peptides. Eleven Th1 epitope-containing peptides common to each serotype were identified in the M protein-derived peptides, and 2 peptides (M-11 and M-12) contained the linear immunodominant antibody-binding epitope. Of the peptides derived from the S, M, and N proteins of FIPV, those that induced significantly stronger Th1 activity than that of the FIPV antigen were rescreened, and 4 peptides were identified. When 3 of these peptides (M-9, I-S2-15, and II-S1-24) were selected and administered with CpG-ODNs to SPF cats, M-9 and II-S1-24 induced Th1 activity. Our results may provide important information for the development of a peptide-based vaccine against FIPV infection.

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Section: Introductionsupporting

confidence: 87%

Section: Sandwich Elisa To Detect Fifn-in Pbmcs Culture Supernatantsmentioning

confidence: 99%

Screening and identification of T helper 1 and linear immunodominant antibody-binding epitopes in spike 1 domain and membrane protein of feline infectious peritonitis virus

Takano

Morioka

Gomi

et al. 2014

Vaccine

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“…Unfortunately, no results were given for cats with FIP. Satoh et al (2011a) developed monoclonal antibodies against feline IFN-γ and used them to study immune responses to FIPV. PBMCs from cats experimentally infected with FIPV that did not develop clinical disease had significantly increased levels of IFN-γ production after exposure to heat-inactivated FIPV compared to cats that died of FIP; the increased IFN-γ levels were more marked in CD8 + than CD4 + T cells.…”

Section: Cytokines and Feline Infectious Peritonitismentioning

confidence: 99%

An update on feline infectious peritonitis: Virology and immunopathogenesis

Pedersen

2014

The Veterinary Journal

178

264

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Feline infectious peritonitis (FIP) continues to be one of the most researched infectious diseases of cats. The relatively high mortality of FIP, especially for younger cats from catteries and shelters, should be reason enough to stimulate such intense interest. However, it is the complexity of the disease and the grudging manner in which it yields its secrets that most fascinate researchers. Feline leukemia virus infection was conquered in less than two decades and the mysteries of feline immunodeficiency virus were largely unraveled in several years. After a half century, FIP remains one of the last important infections of cats for which we have no single diagnostic test, no vaccine and no definitive explanations for how virus and host interact to cause disease. How can a ubiquitous and largely non-pathogenic enteric coronavirus transform into a highly lethal pathogen? What are the interactions between host and virus that determine both disease form (wet or dry) and outcome (death or resistance)? Why is it so difficult, and perhaps impossible, to develop a vaccine for FIP? What role do genetics play in disease susceptibility? This review will explore research conducted over the last 5 years that attempts to answer these and other questions. Although much has been learned about FIP in the last 5 years, the ultimate answers remain for yet more studies.

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“…Multiple studies have led researchers to conclude that immunity to FIPV is largely cell-mediated [4][5][6][7][8]. The potential role of cellular immunity in FIP was also inferred from experiments with cats rendered immunocompromised by chronic experimentally-induced feline immunodeficiency virus (FIV) infection.…”

Section: Introductionmentioning

confidence: 99%

Characterization of antiviral T cell responses during primary and secondary challenge of laboratory cats with feline infectious peritonitis virus (FIPV)

et al. 2019

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Background Feline infectious peritonitis (FIP) is considered highly fatal in its naturally occurring form, although up to 36% of cats resist disease after experimental infection, suggesting that cats in nature may also resist development of FIP in the face of infection with FIP virus (FIPV). Previous experimental FIPV infection studies suggested a role for cell-mediated immunity in resistance to development of FIP. This experimental FIPV infection study in specific pathogen free (SPF) kittens describes longitudinal antiviral T cell responses and clinical outcomes ranging from rapid progression, slow progression, and resistance to disease. Results Differences in disease outcome provided an opportunity to investigate the role of T cell immunity to FIP determined by T cell subset proliferation after stimulation with different viral antigens. Reduced total white blood cell (WBC), lymphocyte and T cell counts in blood were observed during primary acute infection for all experimental groups including cats that survived without clinical FIP. Antiviral T cell responses during early primary infection were also similar between cats that developed FIP and cats remaining healthy. Recovery of antiviral T cell responses during the later phase of acute infection was observed in a subset of cats that survived longer or resisted disease compared to cats showing rapid disease progression. More robust T cell responses at terminal time points were observed in lymph nodes compared to blood in cats that developed FIP. Cats that survived primary infection were challenged a second time to pathogenic FIPV and tested for antiviral T cell responses over a four week period. Nine of ten rechallenged cats did not develop FIP or T cell depletion and all cats demonstrated antiviral T cell responses at multiple time points after rechallenge. Conclusions In summary, definitive adaptive T cell responses predictive of disease outcome were not detected during the early phase of primary FIPV infection. However emergence of antiviral T cell responses after a second exposure to FIPV, implicated cellular immunity in the control of FIPV infection and disease progression. Virus host interactions during very early stages of FIPV infection warrant further investigation to elucidate host resistance to FIP.

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Development of monoclonal antibodies (MAbs) to feline interferon (fIFN)-γ as tools to evaluate cellular immune responses to feline infectious peritonitis virus (FIPV)

Cited by 11 publications

References 40 publications

Screening and identification of T helper 1 and linear immunodominant antibody-binding epitopes in spike 1 domain and membrane protein of feline infectious peritonitis virus

Screening and identification of T helper 1 and linear immunodominant antibody-binding epitopes in spike 1 domain and membrane protein of feline infectious peritonitis virus

An update on feline infectious peritonitis: Virology and immunopathogenesis

Characterization of antiviral T cell responses during primary and secondary challenge of laboratory cats with feline infectious peritonitis virus (FIPV)

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