TY  - JOUR
AU  - Grubor, Nikica M.
AU  - Jovanova-Nešić, Katica
AU  - Shoenfeld, Yehuda
PY  - 2017
UR  - http://intor.torlakinstitut.com/handle/123456789/480
AB  - Cystic echinococcosis (CE) is an infectious disease caused by the larvae of parasite Echinococcus granulosus (E. granulosus). To successfully establish an infection, parasite release some substances and molecules that can modulate host immune functions, stimulating a strong anti-inflammatory reaction to carry favor to host and to reserve self-survival in the host. The literature was reviewed using MEDLINE, and an open access search for immunology of hydatidosis was performed. Accumulating data from animal experiments and human studies provided us with exciting insights into the mechanisms involved that affect all parts of immunity. In this review we used the existing scientific data and discuss how these findings assisted with a better understanding of the immunology of E. granulosus infection in man. The aim of this study is to point the several facts that challenge immune and autoimmune responses to protect E. granulosus from elimination and to minimize host severe pathology. Understanding the immune mechanisms of E. granulosus infection in an intermediate human host will provide, we believe, a more useful treatment with immunomodulating molecules and possibly better protection from parasitic infections. Besides that, the diagnosis of CE has improved due to the application of a new molecular tool for parasite identification by using of new recombinant antigens and immunogenic peptides. More studies for the better understanding of the mechanisms of parasite immune evasion is necessary. It will enable a novel approach in protection, detection and improving of the host inflammatory responses. In contrast, according to the "hygiene hypothesis", clinical applications that decrease the incidence of infection in developed countries and recently in developing countries are at the origin of the increasing incidence of both allergic and autoimmune diseases. Thus, an understanding of the immune mechanisms of E. granulosus infection is extremely important.
PB  - Baishideng Publishing Group Inc, Pleasanton
T2  - World Journal of Hepatology
T1  - Liver cystic echinococcosis and human host immune and autoimmune follow-up: A review
EP  - 1189
IS  - 30
SP  - 1176
VL  - 9
DO  - 10.4254/wjh.v9.i30.1176
ER  - 

@article{
author = "Grubor, Nikica M. and Jovanova-Nešić, Katica and Shoenfeld, Yehuda",
year = "2017",
abstract = "Cystic echinococcosis (CE) is an infectious disease caused by the larvae of parasite Echinococcus granulosus (E. granulosus). To successfully establish an infection, parasite release some substances and molecules that can modulate host immune functions, stimulating a strong anti-inflammatory reaction to carry favor to host and to reserve self-survival in the host. The literature was reviewed using MEDLINE, and an open access search for immunology of hydatidosis was performed. Accumulating data from animal experiments and human studies provided us with exciting insights into the mechanisms involved that affect all parts of immunity. In this review we used the existing scientific data and discuss how these findings assisted with a better understanding of the immunology of E. granulosus infection in man. The aim of this study is to point the several facts that challenge immune and autoimmune responses to protect E. granulosus from elimination and to minimize host severe pathology. Understanding the immune mechanisms of E. granulosus infection in an intermediate human host will provide, we believe, a more useful treatment with immunomodulating molecules and possibly better protection from parasitic infections. Besides that, the diagnosis of CE has improved due to the application of a new molecular tool for parasite identification by using of new recombinant antigens and immunogenic peptides. More studies for the better understanding of the mechanisms of parasite immune evasion is necessary. It will enable a novel approach in protection, detection and improving of the host inflammatory responses. In contrast, according to the "hygiene hypothesis", clinical applications that decrease the incidence of infection in developed countries and recently in developing countries are at the origin of the increasing incidence of both allergic and autoimmune diseases. Thus, an understanding of the immune mechanisms of E. granulosus infection is extremely important.",
publisher = "Baishideng Publishing Group Inc, Pleasanton",
journal = "World Journal of Hepatology",
title = "Liver cystic echinococcosis and human host immune and autoimmune follow-up: A review",
pages = "1189-1176",
number = "30",
volume = "9",
doi = "10.4254/wjh.v9.i30.1176"
}

Grubor, N. M., Jovanova-Nešić, K.,& Shoenfeld, Y.. (2017). Liver cystic echinococcosis and human host immune and autoimmune follow-up: A review. in World Journal of Hepatology
Baishideng Publishing Group Inc, Pleasanton., 9(30), 1176-1189.
https://doi.org/10.4254/wjh.v9.i30.1176

Grubor NM, Jovanova-Nešić K, Shoenfeld Y. Liver cystic echinococcosis and human host immune and autoimmune follow-up: A review. in World Journal of Hepatology. 2017;9(30):1176-1189.
doi:10.4254/wjh.v9.i30.1176 .

Grubor, Nikica M., Jovanova-Nešić, Katica, Shoenfeld, Yehuda, "Liver cystic echinococcosis and human host immune and autoimmune follow-up: A review" in World Journal of Hepatology, 9, no. 30 (2017):1176-1189,
https://doi.org/10.4254/wjh.v9.i30.1176 . .

TY  - JOUR
AU  - Jovanova-Nešić, Katica
AU  - Shoenfeld, Yehuda
AU  - Spector, Novera Herbert
PY  - 2012
UR  - http://intor.torlakinstitut.com/handle/123456789/345
AB  - In the central nervous system (CNS) microglia are crucial for the defense of the brain against invading microorganisms, formation of tumors, and damage following trauma [1]. However, uncontrolled activation of these cells may have deleterious outcomes [2] through activation of Fcγ and the complement 3 receptors and the induction of an adaptive immune reaction [3]. Proteins contributing to this reaction are the intercellular adhesion molecule-1 (ICAM-1) [3] and CD3 molecules, among others. Both can be expressed on the glia cells before cytokine release and may facilitate an autoimmune inflammatory reaction in the brain. Round microglial cells among the pyramidal cells of the hippocampus with increased expression of CD32+ (FcγIIa) and near the site of injection of aluminum were detected immunohistochemically and indicate microglial activation at the site of aluminum injury. ICAM-1+ immunoreactivity significantly increased in the hippocampus and in the choroids plexus, indicating increased inflammation in the brain as well as increased CD3ε+ expression in the hippocampus and non-MHC-restricted T cytotoxicity after aluminum injection. The pattern of expression of CD32+ (FcγIIa receptor) near the site of aluminum injection indicates that microglia may play a phagocytic role at the site of aluminum-induced excitotoxicity in the brain. Significant expression of ICAM-1+ and CD3ε + immunoreactive cells with the clusters of ICAM-1+ in the choroid plexus suggests a consequently neurotoxic autoimmune reaction induced by microglial hyperactivation in the injured brain.
T2  - Current Aging Science
T1  - Aluminum excytotoxicity and neuroautotoimmunity: The role of the brain expression of CD32+ (FcγRIIa), ICAM-1+ and CD3ε in aging
EP  - 217
IS  - 3
SP  - 209
VL  - 5
DO  - 10.2174/1874609811205030007
ER  - 

@article{
author = "Jovanova-Nešić, Katica and Shoenfeld, Yehuda and Spector, Novera Herbert",
year = "2012",
abstract = "In the central nervous system (CNS) microglia are crucial for the defense of the brain against invading microorganisms, formation of tumors, and damage following trauma [1]. However, uncontrolled activation of these cells may have deleterious outcomes [2] through activation of Fcγ and the complement 3 receptors and the induction of an adaptive immune reaction [3]. Proteins contributing to this reaction are the intercellular adhesion molecule-1 (ICAM-1) [3] and CD3 molecules, among others. Both can be expressed on the glia cells before cytokine release and may facilitate an autoimmune inflammatory reaction in the brain. Round microglial cells among the pyramidal cells of the hippocampus with increased expression of CD32+ (FcγIIa) and near the site of injection of aluminum were detected immunohistochemically and indicate microglial activation at the site of aluminum injury. ICAM-1+ immunoreactivity significantly increased in the hippocampus and in the choroids plexus, indicating increased inflammation in the brain as well as increased CD3ε+ expression in the hippocampus and non-MHC-restricted T cytotoxicity after aluminum injection. The pattern of expression of CD32+ (FcγIIa receptor) near the site of aluminum injection indicates that microglia may play a phagocytic role at the site of aluminum-induced excitotoxicity in the brain. Significant expression of ICAM-1+ and CD3ε + immunoreactive cells with the clusters of ICAM-1+ in the choroid plexus suggests a consequently neurotoxic autoimmune reaction induced by microglial hyperactivation in the injured brain.",
journal = "Current Aging Science",
title = "Aluminum excytotoxicity and neuroautotoimmunity: The role of the brain expression of CD32+ (FcγRIIa), ICAM-1+ and CD3ε in aging",
pages = "217-209",
number = "3",
volume = "5",
doi = "10.2174/1874609811205030007"
}

Jovanova-Nešić, K., Shoenfeld, Y.,& Spector, N. H.. (2012). Aluminum excytotoxicity and neuroautotoimmunity: The role of the brain expression of CD32+ (FcγRIIa), ICAM-1+ and CD3ε in aging. in Current Aging Science, 5(3), 209-217.
https://doi.org/10.2174/1874609811205030007

Jovanova-Nešić K, Shoenfeld Y, Spector NH. Aluminum excytotoxicity and neuroautotoimmunity: The role of the brain expression of CD32+ (FcγRIIa), ICAM-1+ and CD3ε in aging. in Current Aging Science. 2012;5(3):209-217.
doi:10.2174/1874609811205030007 .

Jovanova-Nešić, Katica, Shoenfeld, Yehuda, Spector, Novera Herbert, "Aluminum excytotoxicity and neuroautotoimmunity: The role of the brain expression of CD32+ (FcγRIIa), ICAM-1+ and CD3ε in aging" in Current Aging Science, 5, no. 3 (2012):209-217,
https://doi.org/10.2174/1874609811205030007 . .

TY  - JOUR
AU  - Jovanova-Nešić, Katica
AU  - Koruga, D.
AU  - Kojić, D.
AU  - Kostić, V.
AU  - Rakić, L.
AU  - Shoenfeld, Yehuda
PY  - 2009
UR  - http://intor.torlakinstitut.com/handle/123456789/291
AB  - Experimental autoimmune encephalomyelitis (EAE) induced by ventricular injection of antimyelin oligodendrocyte antibodies in DA rats showed severe clinical signs 4 to 5 days after injection. Immunocytochemically, connexin 43 (Cx43) expression increased in the choroid plexus and in the subventricular and subgranular zones of the hippocampus during the development of acute EAE, and decreased after the beginning of the remission phase of the disease. Quantitative computing analysis showed a significantly increased Cx43 expression in the choroid plexus at the peak of the disease. Plaque-pattern expression of the Cx43 in the choroid plexus (CP) of acute EAE correlated with the increased docking and coupling of the Cx43 hemichannels revealed by atomic force microscopy (AFM). The inner diameter of the gap junction (GJ) channels decreased in the CP of acute EAE, measured by AFM. Cell structure conformational changes showed influences the channels' flexibility in acute EAE.
PB  - Wiley-Blackwell, Malden
T2  - Contemporary Challenges in Autoimmunity
T1  - Choroid Plexus Connexin 43 Expression and Gap Junction Flexibility Are Associated with Clinical Features of Acute EAE
EP  - 82
SP  - 75
VL  - 1173
DO  - 10.1111/j.1749-6632.2009.04658.x
ER  - 

@article{
author = "Jovanova-Nešić, Katica and Koruga, D. and Kojić, D. and Kostić, V. and Rakić, L. and Shoenfeld, Yehuda",
year = "2009",
abstract = "Experimental autoimmune encephalomyelitis (EAE) induced by ventricular injection of antimyelin oligodendrocyte antibodies in DA rats showed severe clinical signs 4 to 5 days after injection. Immunocytochemically, connexin 43 (Cx43) expression increased in the choroid plexus and in the subventricular and subgranular zones of the hippocampus during the development of acute EAE, and decreased after the beginning of the remission phase of the disease. Quantitative computing analysis showed a significantly increased Cx43 expression in the choroid plexus at the peak of the disease. Plaque-pattern expression of the Cx43 in the choroid plexus (CP) of acute EAE correlated with the increased docking and coupling of the Cx43 hemichannels revealed by atomic force microscopy (AFM). The inner diameter of the gap junction (GJ) channels decreased in the CP of acute EAE, measured by AFM. Cell structure conformational changes showed influences the channels' flexibility in acute EAE.",
publisher = "Wiley-Blackwell, Malden",
journal = "Contemporary Challenges in Autoimmunity",
title = "Choroid Plexus Connexin 43 Expression and Gap Junction Flexibility Are Associated with Clinical Features of Acute EAE",
pages = "82-75",
volume = "1173",
doi = "10.1111/j.1749-6632.2009.04658.x"
}

Jovanova-Nešić, K., Koruga, D., Kojić, D., Kostić, V., Rakić, L.,& Shoenfeld, Y.. (2009). Choroid Plexus Connexin 43 Expression and Gap Junction Flexibility Are Associated with Clinical Features of Acute EAE. in Contemporary Challenges in Autoimmunity
Wiley-Blackwell, Malden., 1173, 75-82.
https://doi.org/10.1111/j.1749-6632.2009.04658.x

Jovanova-Nešić K, Koruga D, Kojić D, Kostić V, Rakić L, Shoenfeld Y. Choroid Plexus Connexin 43 Expression and Gap Junction Flexibility Are Associated with Clinical Features of Acute EAE. in Contemporary Challenges in Autoimmunity. 2009;1173:75-82.
doi:10.1111/j.1749-6632.2009.04658.x .

Jovanova-Nešić, Katica, Koruga, D., Kojić, D., Kostić, V., Rakić, L., Shoenfeld, Yehuda, "Choroid Plexus Connexin 43 Expression and Gap Junction Flexibility Are Associated with Clinical Features of Acute EAE" in Contemporary Challenges in Autoimmunity, 1173 (2009):75-82,
https://doi.org/10.1111/j.1749-6632.2009.04658.x . .

TY  - CONF
AU  - Jovanova-Nešić, Katica
AU  - Shoenfeld, Yehuda
PY  - 2007
UR  - http://intor.torlakinstitut.com/handle/123456789/237
AB  - The aim of the study is to explore the relationship between leakage of the blood-brain barrier and inflammation, the reason why demyelination occurs - seemingly in the absence of an antigen-specific immune response that requires explanation if a coherent account of an inflammatory-mediated demyelination is to be achieved. In this study the cellular biology of the glial cells important for the synthesis and maintenance of central nervous system (CNS) myelin and their inter-relations with other environmental cells (neuronal, microglial, olygodendroglial, astrocytes, endothelial, epithelial, T lymphocytes, B lymphocytes, monocytes, and macrophages) and with the compound of the extracellular matrix (ECM) during the development of an autoimmune inflammatory and demyelinating processes in the brain was analyzed. Upon activation in the peripheral tissue, immune cells reach their target organ via bloodstream and interacting with blood vessels wall components in the absence of exogenous stimulus mount an attack against the local milleu, which is the starting point of a pathogenic inflammatory reaction. Each of these contacts may trigger profuse secretion of cytokines, chemokines, and other soluble inflammatory mediators, which in the CNS by activating of local glial cells and by attracting and stimulating blood-borne monocyte/macrophages can act directly on neural cells and will cause their demyelination.
PB  - Blackwell Publishing Inc.
C3  - Annals of the New York Academy of Sciences
T1  - Autoimmunity in the brain: The pathogenesis insight from cell biology
EP  - 154
SP  - 142
VL  - 1107
DO  - 10.1196/annals.1381.016
ER  - 

@conference{
author = "Jovanova-Nešić, Katica and Shoenfeld, Yehuda",
year = "2007",
abstract = "The aim of the study is to explore the relationship between leakage of the blood-brain barrier and inflammation, the reason why demyelination occurs - seemingly in the absence of an antigen-specific immune response that requires explanation if a coherent account of an inflammatory-mediated demyelination is to be achieved. In this study the cellular biology of the glial cells important for the synthesis and maintenance of central nervous system (CNS) myelin and their inter-relations with other environmental cells (neuronal, microglial, olygodendroglial, astrocytes, endothelial, epithelial, T lymphocytes, B lymphocytes, monocytes, and macrophages) and with the compound of the extracellular matrix (ECM) during the development of an autoimmune inflammatory and demyelinating processes in the brain was analyzed. Upon activation in the peripheral tissue, immune cells reach their target organ via bloodstream and interacting with blood vessels wall components in the absence of exogenous stimulus mount an attack against the local milleu, which is the starting point of a pathogenic inflammatory reaction. Each of these contacts may trigger profuse secretion of cytokines, chemokines, and other soluble inflammatory mediators, which in the CNS by activating of local glial cells and by attracting and stimulating blood-borne monocyte/macrophages can act directly on neural cells and will cause their demyelination.",
publisher = "Blackwell Publishing Inc.",
journal = "Annals of the New York Academy of Sciences",
title = "Autoimmunity in the brain: The pathogenesis insight from cell biology",
pages = "154-142",
volume = "1107",
doi = "10.1196/annals.1381.016"
}

Jovanova-Nešić, K.,& Shoenfeld, Y.. (2007). Autoimmunity in the brain: The pathogenesis insight from cell biology. in Annals of the New York Academy of Sciences
Blackwell Publishing Inc.., 1107, 142-154.
https://doi.org/10.1196/annals.1381.016

Jovanova-Nešić K, Shoenfeld Y. Autoimmunity in the brain: The pathogenesis insight from cell biology. in Annals of the New York Academy of Sciences. 2007;1107:142-154.
doi:10.1196/annals.1381.016 .

Jovanova-Nešić, Katica, Shoenfeld, Yehuda, "Autoimmunity in the brain: The pathogenesis insight from cell biology" in Annals of the New York Academy of Sciences, 1107 (2007):142-154,
https://doi.org/10.1196/annals.1381.016 . .