Reciprocal Change With Age in Antibody to Extrinsic and Intrinsic Antigens

Rowley, M. J.; Buchanan, Heather; Mackay, I. R.

doi:10.1016/s0140-6736(68)92893-6

Cited by 141 publications

(57 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…An effect of therapy on DNA binding has also been suggested by others (3). The increasing levels of DNA binding with increasing age in the control subjects suggests that these antibodies are an acquired property similar to the results of age-related studies of antiglobulin and antinuclear antibodies (18).…”

Section: Discussionsupporting

confidence: 67%

“…Of these 10, nine binding levels than normal subjects. Table were under 18 years of age, consistent with 1 lists the diagnoses in patients in the non-the suggestion that DNA antibody activity SLE group with binding levels greater than is an acquired characteristic similar to the age-related observations of antinuclear and antiglobulin antibody activity (18). As a further example of DNA binding in non-SLE patients, a group of patients with Graves' disease (studied in collaboration with Dr. Sidney Werner) had levels of binding above the normal range ( Figure 2).…”

Section: Clinical Studiessupporting

confidence: 73%

See 1 more Smart Citation

Serum DNA binding activity in healthy subjects and in rheumatic disease

Hasselbacher

LeRoy

1974

Arthritis & Rheumatism

View full text Add to dashboard Cite

Modifications of the Farr ammonium sulfate precipitation assay for DNA antibodies have increased sensitivity and led to the detection of DNA binding in the sera of healthy subjects and subjects with rheumatic disease other than systemic lupus erythematosus (SLE). The presence of binding in immunochemically pure IgG and the pattern of inhibition by native and denatured DNA support the thesis that DNA binding of normal, non‐SLE, and SLE sera is antibody and similar in kind although not in degree. The presence of antibodies to DNA in normal and non‐SLE sera may limit the qualitative role of these antibodies in SLE and render DNA antibodies similar to antiglobulin and other antinuclear antibodies in rheumatic disease.

show abstract

Section: Discussionsupporting

confidence: 67%

Section: Clinical Studiessupporting

confidence: 73%

Serum DNA binding activity in healthy subjects and in rheumatic disease

Hasselbacher

LeRoy

1974

Arthritis & Rheumatism

View full text Add to dashboard Cite

show abstract

“…In contrast to progressive decline in immune functions with advancing age, there is an increased reactivity to self and endogenous antigens as evidenced by the presence and increased titers of a variety of autoantibodies [8][9][10][11][12], which suggest a loss of peripheral tolerance in aging. The information regarding mechanisms of impaired tolerance in human aging is limited.…”

Section: Autoimmunity In Aging Role Of Apoptosis In Autoimmunity In Amentioning

confidence: 99%

“…Aged humans develop a variety of autoantibodies, and display poor response to vaccines and increased susceptibility to both viral and bacterial infections. The progressive impairment in immune functions include progressive T cell deficiency, which is contributed by thymic involution [1], increased apoptosis of T cells and T cell subsets [2][3][4], and impaired priming of T cells by DCs [5][6][7]; B cell dysfunctions are revealed by impaired specific antibody response to vaccines, and development of autoimmunity [8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Role of Dendritic Cells in Autoimmunity in Aged Humans

Gupta¹

2014

Immunome Res

View full text Add to dashboard Cite

Immunological tolerance to self-antigen is mediated by deletion of self-reactive lymphocytes by apoptosis, unresponsiveness to self-antigens (anergy), regulation by T cells (Treg), and efficient removal of apoptotic bodies by phagocytic cells. Dendritic cells (DCs) play an important role in both tolerance (predominantly via induction of Treg) and inthe induction of immune response to non-self antigens. Therefore, an impairment of DCs functions may result in the loss of tolerance and induction of immune response to self-antigens, resulting in autoimmunity. Aging represents a paradox of impaired response to non-self antigens, and an increased response to self-antigens, resulting in an increased susceptibility to infections, and development of autoimmunity in aged humans. I have reviewed the role of DCs and mechanisms involved in autoimmunity, including epigenetic changes in aged DNA, and histone modifications in chromatin in human aging.

show abstract

“…Decreased mature B cell turnover, hence increased lifespan [87,112] Increased number and proportion of ABCs [15,16] Immune responses Fewer GCs and PCs following T-dependent immunization [108,[113][114][115] Defects in T helper function [33][34][35] No change in PCs following T-independent immunization [116] Increased prevalence of chronically activated B cells [117] Increased prevalence of PCs secreting autoantibodies [117][118][119][120] Impaired class switching [109,121] [59]. During TR selection, sustained or strong BCR signals yield death or inactivation [55,[60][61][62][63][64].…”

Section: Constant Mature B Cell Numbersmentioning

confidence: 99%

New Cells in Old Mice: The ABCs of Humoral Immunosenescence

Hao¹,

Oropallo²,

Scholz³

et al. 2012

TOLSJ

View full text Add to dashboard Cite

Dampened humoral immune responses and increased propensity for autoimmune and inflammatory diseases are hallmarks of aging. Here, we summarize recent progress in understanding how aging affects humoral immunity, focusing on the discovery of a phenotypically and functionally unique B cell subset in aged mice, its potential role in immunosenescence, and its relationship to increased inflammation and autoimmunity.Keywords: Age, B cell homeostasis, function. OVERVIEWAging is a complex process characterized by functional declines in multiple physiologic systems. Age-related alterations in the immune system, a spectrum of changes that are in toto termed "immunosenescence," yield enhanced susceptibility to infectious diseases, increased propensity for inflammatory responses and autoantibody production, and consequently, increased morbidity and mortality [1][2][3][4][5][6][7][8][9][10][11][12][13][14]. Understanding the mechanisms through which age-associated phenomena yield the overall immunosenescent phenotype presents a fundamental and challenging biological problem. Multiple factors contribute to this general deterioration of immune activity, encompassing both cell-intrinsic changes and alterations in lymphoid organ microenvironments. In particular, determining how age-associated changes result in modified homeostatic relationships among steady-state lymphocyte pools, and how this in turn impacts the initiation and quality of adaptive immune responses, may provide the keys to effective prophylaxis and intervention. In this review, we briefly summarize global shifts in humoral immune responsiveness that emerge with age, followed by a detailed consideration of changes in the genesis and homeostasis of B lymphocyte populations. Finally, we focus on a recently described B lineage subset that emerges with age [15,16], and discuss how the shifting palette of functional B cell subsets may contribute to the global landscape of immunosenescence. AGING ALTERS HUMORAL IMMUNE RESPONSESProtective humoral immunity requires maintaining both naïve and antigen-experienced B cell subsets that respond robustly to pathogens, yet maintain self-tolerance. Multiple studies have revealed that, in contrast to healthy young adults, aged individuals display blunted humoral responses to both new and previously encountered antigens, as well as increases in autoantibody levels [4,7,11,13,[17][18][19]. Accordingly, studies over the last several decades have interrogated the basis for this array of features. Table I summarizes some of the changes in B cell development, dynamics and function that have been revealed by these efforts.Early work focused primarily upon whether the frequency or clonal composition of responsive B cells changes in aged individuals, as well as whether hallmarks of effective humoral immune responses are altered. Examinations of how aging influences responding B cell frequencies, using model antigens in mice, have yielded mixed results. For example, aged mice have decreased frequencies of B cells responsive to some...

show abstract

Reciprocal Change With Age in Antibody to Extrinsic and Intrinsic Antigens

Cited by 141 publications

References 4 publications

Serum DNA binding activity in healthy subjects and in rheumatic disease

Serum DNA binding activity in healthy subjects and in rheumatic disease

Role of Dendritic Cells in Autoimmunity in Aged Humans

New Cells in Old Mice: The ABCs of Humoral Immunosenescence

Contact Info

Product

Resources

About