Conditions Determining the Transplantability of Tissues in the Brain

Murphy, James B.; Sturm, Ernest

doi:10.1084/jem.38.2.183

Cited by 209 publications

(84 citation statements)

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“…In the early years of the twentieth century, Murphy and Sturm (202) proposed two possible explanations: (i) mechanical impediment of cells to migrate beyond the perivascular spaces; (ii) lymphoid cells find the brain tissue an uncongenial environment. These authors were the first to define BBB as an ''anatomic barrier that restricts diapedesis'' and ensures the immune privileged state of the brain.…”

Section: Bbb Permeability Is Altered By Ros Enabling Homing Ofmentioning

confidence: 99%

Redox Control of Microglial Function: Molecular Mechanisms and Functional Significance

Rojo

McBean²,

Cindrić³

et al. 2014

Antioxidants & Redox Signaling

262

242

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Neurodegenerative diseases are characterized by chronic microglial over-activation and oxidative stress. It is now beginning to be recognized that reactive oxygen species (ROS) produced by either microglia or the surrounding environment not only impact neurons but also modulate microglial activity. In this review, we first analyze the hallmarks of pro-inflammatory and anti-inflammatory phenotypes of microglia and their regulation by ROS. Then, we consider the production of reactive oxygen and nitrogen species by NADPH oxidases and nitric oxide synthases and the new findings that also indicate an essential role of glutathione (c-glutamyl-lcysteinylglycine) in redox homeostasis of microglia. The effect of oxidant modification of macromolecules on signaling is analyzed at the level of oxidized lipid by-products and sulfhydryl modification of microglial proteins. Redox signaling has a profound impact on two transcription factors that modulate microglial fate, nuclear factor kappa-light-chain-enhancer of activated B cells, and nuclear factor (erythroid-derived 2)-like 2, master regulators of the pro-inflammatory and antioxidant responses of microglia, respectively. The relevance of these proteins in the modulation of microglial activity and the interplay between them will be evaluated. Finally, the relevance of ROS in altering blood brain barrier permeability is discussed. Recent examples of the importance of these findings in the onset or progression of neurodegenerative diseases are also discussed. This review should provide a profound insight into the role of redox homeostasis in microglial activity and help in the identification of new promising targets to control neuroinflammation through redox control of the brain.

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Section: Bbb Permeability Is Altered By Ros Enabling Homing Ofmentioning

confidence: 99%

Redox Control of Microglial Function: Molecular Mechanisms and Functional Significance

Rojo

McBean²,

Cindrić³

et al. 2014

Antioxidants & Redox Signaling

262

242

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“…Back then, Y Shirai observed that rat sarcoma grew well when transplanted into the mouse brain parenchyma, but not when implanted subcutaneously or intramuscularly [2]. Murphy and Strum extended these findings in 1923 by demonstrating that if recipient spleen was cotransplanted with the foreign tumour in the brain parenchyma, it inhibited the tumour growth [3]. This showed that the survival of the foreign tumour within the brain parenchyma was occurring as a result of disconnection from the systemic immune system.…”

Section: Immune Privilege Down the Agesmentioning

confidence: 99%

What is the blood–brain barrier (not)?

Bechmann

Galea

Perry

2007

Trends in Immunology

466

383

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(preferred mode of contact) This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. The immune privilege of the central nervous system is indispensable for damage limitation during inflammation in a sensitive organ with poor regenerative capacity.It is a longstanding notion which has down the years acquired a lack of precision in its definition and a number of misconceptions. In this article we address these issues and re-define CNS immune privilege in the light of recent data. We show how it is far from absolute and how it varies with age and brain region. Immune privilege in the CNS is often mis-attributed wholly to the blood-brain barrier. We discuss the pivotal role of the specialization of the brain's afferent arm in adaptive immunity, which results in a lack of cell-mediated antigen drainage to the cervical lymph nodes although soluble drainage to these nodes is well described. It is now increasingly recognized how immune privilege is actively maintained as a result of the immunoregulatory characteristics of the CNS resident cells and their microenvironment. Immune privilege down the agesPrivilege: "a right, advantage, or immunity granted to or enjoyed by a person, or class of persons, beyond the common advantages of others" [1].The concept of "immune privilege" in the central nervous system (CNS) has a long history. That antigens trapped within the brain parenchyma evade systemic immunological recognition has been shown as early as 1921 in Japan. Back then, Y Shirai observed that rat sarcoma grew well when transplanted into the mouse brain parenchyma, but not when implanted subcutaneously or intramuscularly [2]. Murphy and Strum extended these findings in 1923 by demonstrating that if recipient spleen was cotransplanted with the foreign tumour in the brain parenchyma, it inhibited the tumour growth [3]. This showed that the survival of the foreign tumour within the brain parenchyma was occurring as a result of disconnection from the systemic immune system. These were the first indications of what was later to be termed "immunological privilege" by Billingham and Boswell [4]. Over the years, these observations have been shown to hold true for tissue grafts [5], bacteria [6], viruses [7] and vectors [8], which all evaded immune recognition when delivered to the brain parenchyma. Around the same time as the brain's "immune privilege" was being discovered, the blood-brain barrier (BBB) was under study, and the two concepts grew together. This had two consequences.First, the brain's "immune privilege" assumed a more absolute meaning, rendering it too strong a descriptive term for the brain's relationship with the immune system (Box 1).Secondly, "immune privilege" was inappropriately wholly attributed to the BBB (see previous article), whereas other features such as the specialization of afferent communication from CNS to nearby lymphatic organs and the nature of the CNS microenvironment are much more pertinent (Box 1). In this article, we aim to upd...

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“…Murphy, J.B., et al [59] have studied mouse sarcoma tissue, which was found not to be rejected implantation into rat brain and given their views that the CNS was exempt from the immunological processes responsible for graft rejection. Sabin, F.R.…”

Section: Introductionmentioning

confidence: 99%

Role of Complements and Immunoglobulins in Duchenne Muscular Dystrophy

Kumar¹,

Mittal²,

nbsp³

et al. 2014

OJAppS

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Muscular dystrophies are myopathies and tend to progressive, with ongoing degeneration and regeneration of muscle fibers. Spinal muscular atrophy (SMA), amyotrophic lateral sclerosis (ALS) and polio myelitis are essentially diseases of the anterior horn cells of the spine. It has been reported in literature that humoral immunity is manifested by the antibodies production. These are special chemical substances that react against foreign body. Antibodies are serum proteins, which are immunoglobulins and possess antibody activity and are classified according to antigens and stimulate their production such as IgA, JgG, IgM, IgD and IgE. All the immunological parameters such as of C3, C4, IgG, IgM and IgA, which are measured in Duchenne muscular dystrophy go down in comparison to healthy subjects. Complement C3 and Complement C4 go down about 44.3% and 78.57% respectively from the normal values. The serum IgG, IgM and IgA levels were also go down about 65%, 84% and 99.56% respectively in comparison to healthy subjects. A trend between all the immunoglobulins has been set up and it is rAG.M > rMA.G. > rGM.A, while we have a trend in DMD cases is rMA.G. > rAG.M > rGM.A. We are in a position to say that our data have a relevance of high authenticity and reliability to accept that there is a deficit in immunity in DMD cases. The deficit in immunity may be a cause to damage muscle for abnormal functioning.

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Conditions Determining the Transplantability of Tissues in the Brain

Cited by 209 publications

References 3 publications

Redox Control of Microglial Function: Molecular Mechanisms and Functional Significance

Redox Control of Microglial Function: Molecular Mechanisms and Functional Significance

What is the blood–brain barrier (not)?

Role of Complements and Immunoglobulins in Duchenne Muscular Dystrophy

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