scholarly journals Recombinant protein of Haemonchus contortus small GTPase ADP-ribosylation factor 1 (HcARF1) modulate the cell mediated immune response in vitro

Oncotarget ◽  
2017 ◽  
Vol 8 (68) ◽  
pp. 112211-112221 ◽  
Author(s):  
Javaid Ali Gadahi ◽  
Muhammad Ehsan ◽  
Shuai Wang ◽  
Zhenchao Zhang ◽  
Ruofeng Yan ◽  
...  
Vaccines ◽  
2020 ◽  
Vol 8 (4) ◽  
pp. 726
Author(s):  
Muhammad Waqqas Hasan ◽  
Muhammad Haseeb ◽  
Muhammad Ehsan ◽  
Javaid Ali Gadahi ◽  
Muhammad Ali-ul-Husnain Naqvi ◽  
...  

ADP-ribosylation factor 1 (HcARF1) is one of the Haemonchus contortus (H. contortus) excretory/secretory proteins involved in modulating the immune response of goat peripheral blood mononuclear cells (PBMC). Here, we evaluated the immunogenic potential of recombinant HcARF1 (rHcARF1) against H. contortus infection in Institute of Cancer Research (ICR) mice. Briefly, rHcARF1 was entrapped in poly (D, L-lactide-co-glycolide) (PLGA) and chitosan (CS) nanoparticles (NP) and injected into mice as a vaccine. Fifty-six ICR mice were assigned randomly into seven groups, with eight animals in each group, and they were vaccinated subcutaneously. At the end of the experiment (14th day), the blood and the spleen were collected from euthanized mice to detect lymphocyte proliferation, cytokine analysis, and the production of antigen-specific antibodies. Scanning electron microscope was used to determine the size, morphology, and zeta potential of nanoparticles. Flow cytometry was performed, which presented the increase percentages of CD4+ T cells (CD3e+CD4+), CD8+ T cells (CD3e+CD8+) and dendritic cells (CD11c+CD83+, CD11c+CD86+) in mice vaccinated with rHcARF1+PLGA NP. Immunoassay analysis show raised humoral (Immunoglobulin (Ig)G1, IgG2a, IgM) and cell-mediated immune response (Interleukin (IL)-4, IL-12, and IL-17, and Interferon (IFN)-γ) induced by rHcARF1+PLGA NP. Experimental groups that were treated with the antigen-loaded NP yield higher lymphocyte proliferation than the control groups. Based on these results, we could propose that the rHcARF1 encapsulated in NP could stimulate a strong immune response in mice rather than administering alone against the infection of H. contortus.


2007 ◽  
Vol 7 (9) ◽  
pp. 1211-1220 ◽  
Author(s):  
Dragana Vucevic ◽  
Eleni Melliou ◽  
Sasa Vasilijic ◽  
Sonja Gasic ◽  
Petar Ivanovski ◽  
...  

1970 ◽  
Vol 4 (5) ◽  
pp. 437-437
Author(s):  
Samuel P Gotoff ◽  
Somsak Lolekha

2007 ◽  
Vol 142 (1) ◽  
pp. 66-71 ◽  
Author(s):  
Andrzej Gryglewski ◽  
Pawel Majcher ◽  
Krzysztof Bryniarski ◽  
Stanislaw Konturek ◽  
Maria Ptak ◽  
...  

1972 ◽  
Vol 3 (3) ◽  
pp. 405-420 ◽  
Author(s):  
Hermann Wagner ◽  
Marc Feldmann

1972 ◽  
Vol 136 (2) ◽  
pp. 331-343 ◽  
Author(s):  
Hermann Wagner ◽  
Marc Feldmann ◽  
W. Boyle ◽  
J. W. Schrader

All efficient cell separation procedure and specific anti-macrophage serum were used to investigate the requirement of macrophages in the in vitro allograft response of mouse lymphoid cells. The efficiency of the macrophage-depletion procedure used and the undiminished capacity of the purified lymphocytes to respond were verified by also testing the antibody responses to sheep red cells (SRC) and dinitrophenylated polymeric flagellin (DNP POL) as well as the proliferative response to allogeneic cells. It was found that the generation of cytotoxic lymphocytes were diminished after macrophage depletion by surface adherence. The combination of anti-macrophage serum and column purification resulted in the total abolition of cytotoxic activity. The cell-mediated immune response was restored completely by addition of peritoneal macrophages, with as few as 1 macrophage to 600 lymphocytes permitting a significant restoration. Macrophages were not involved in the cytotoxic effector phase, but were essential in immune induction. A subcellular H-2 alloantigen preparation was only immunogenic in the presence of macrophages, indicating that a mere reduction in the size of the antigen from cell-bound alloantigens to membrane fragments was not the sole function of macrophages. The results suggest that macrophages collaborate with T cells in the initiation of an allograft response in vitro.


2004 ◽  
Vol 279 (50) ◽  
pp. 52735-52743 ◽  
Author(s):  
Mark A. Ellis ◽  
Mark T. Miedel ◽  
Christopher J. Guerriero ◽  
Ora A. Weisz

Polarized epithelial cells efficiently sort newly synthesized apical and basolateral proteins into distinct transport carriers that emerge from thetrans-Golgi network (TGN), and this sorting is recapitulated in nonpolarized cells. While the targeting signals of basolaterally destined proteins are generally cytoplasmically disposed, apical sorting signals are not typically accessible to the cytosol, and the transport machinery required for segregation and export of apical cargo remains largely unknown. Here we investigated the molecular requirements for TGN export of the apical marker influenza hemagglutinin (HA) in HeLa cells using anin vitroreconstitution assay. HA was released from the TGN in intact membrane-bound compartments, and export was dependent on addition of an ATP-regenerating system and exogenous cytosol. HA release was inhibited by guanosine 5′-O-(3-thiotriphosphate) (GTPγS) as well as under conditions known to negatively regulate apical transportin vivo, including expression of the acid-activated proton channel influenza M2. Interestingly, release of HA was unaffected by depletion of ADP-ribosylation factor 1, a small GTPase that has been implicated in the recruitment of all known adaptors and coat proteins to the Golgi complex. Furthermore, regulation of HA release by GTPγS or M2 expression was unaffected by cytosolic depletion of ADP-ribosylation factor 1, suggesting that HA sorting remains functionally intact in the absence of the small GTPase. These data suggest that TGN sorting and export of influenza HA does not require classical adaptors involved in the formation of other classes of exocytic carriers and thus appears to proceed via a novel mechanism.


1972 ◽  
Vol 4 (1) ◽  
pp. 39-50 ◽  
Author(s):  
Hermann Wagner ◽  
Alan W. Harris ◽  
Marc Feldmann

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