Plants in their natural habitats adapt to drought stress in the environment through a variety of mechanisms, ranging from transient responses to low soil moisture to major survival mechanisms of escape by early flowering in absence of seasonal rainfall. However, crop plants selected by humans to yield products such as grain, vegetable, or fruit in favorable environments with high inputs of water and fertilizer are expected to yield an economic product in response to inputs. Crop plants selected for their economic yield need to survive drought stress through mechanisms that maintain crop yield. Studies on model plants for their survival under stress do not, therefore, always translate to yield of crop plants under stress, and different aspects of drought stress response need to be emphasized. The crop plant model rice ( Oryza sativa) is used here as an example to highlight mechanisms and genes for adaptation of crop plants to drought stress.

Plant adaptation to drought stress.

Antibodies that recognize and bind to DNA (anti-DNA antibodies) are serological hallmarks of systemic lupus erythematosus (SLE) and key markers for diagnosis and disease activity. In addition to common use in the clinic, anti-DNA antibody testing now also determines eligibility for clinical trials, raising important questions about the nature of the antibody-antigen interaction. At present, no 'gold standard' for serological assessment exists, and anti-DNA antibody binding can be measured with a variety of assay formats, which differ in the nature of the DNA substrates and in the conditions for binding and detection of antibodies. A mechanism called monogamous bivalency--in which high avidity results from simultaneous interaction of IgG Fab sites with a single polynucleotide chain--determines anti-DNA antibody binding; this mechanism might affect antibody detection in different assay formats. Although anti-DNA antibodies can promote pathogenesis by depositing in the kidney or driving cytokine production, they are not all alike, pathologically, and anti-DNA antibody expression does not necessarily correlate with active disease. Levels of anti-DNA antibodies in patients with SLE can vary over time, distinguishing anti-DNA antibodies from other pathogenic antinuclear antibodies. Elucidation of the binding specificities and the pathogenic roles of anti-DNA antibodies in SLE should enable improvements in the design of informative assays for both clinical and research purposes.

Anti-DNA antibodies--quintessential biomarkers of SLE.

Following fifteen years of research, neutrophil extracellular traps (NETs) are widely reported in a large range of inflammatory infectious and non-infectious diseases. Cumulating evidences from in vitro, in vivo and clinical diagnostics suggest that NETs may play a crucial role in inflammation and autoimmunity in a variety of autoimmune diseases, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV). Most likely, NETs contribute to breaking self-tolerance in autoimmune diseases in several ways. During this review, we discuss the current knowledge on how NETs could drive autoimmune responses. NETs can break self-tolerance by being a source of autoantigens for autoantibodies found in autoimmune diseases, such as anti-citrullinated protein antibodies (ACPAs) in RA, anti-dsDNA in SLE and anti-myeloperoxidase and anti-protein 3 in AAV. Moreover, NET components could accelerate the inflammatory response by mediating complement activation, acting as danger-associated molecular patterns (DAMPs) and inflammasome activators, for example. NETs also can activate other immune cells, such as B cells, antigen-presenting cells and T cells. Additionally, impaired clearance of NETs in autoimmune diseases prolongs the presence of active NETs and their components and, in this way, accelerate immune responses. NETs have not only been implicated as drivers of inflammation, but also are linked to resolution of inflammation. Therefore, NETs may be central regulators of inflammation and autoimmunity, serve as biomarkers, as well as promising targets for future therapeutics of inflammatory autoimmune diseases.

https://www.mdpi.com/2073-4409/9/4/915/pdf

Neutrophil Extracellular Traps (NETs) Take the Central Stage in Driving Autoimmune Responses

The immune system and the kidneys are closely linked. In health the kidneys contribute to immune homeostasis, while components of the immune system mediate many acute forms of renal disease and play a central role in progression of chronic kidney disease. A dysregulated immune system can have either direct or indirect renal effects. Direct immune-mediated kidney diseases are usually a consequence of autoantibodies directed against a constituent renal antigen, such as collagen IV in anti-glomerular basement membrane disease. Indirect immune-mediated renal disease often follows systemic autoimmunity with immune complex formation, but can also be due to uncontrolled activation of the complement pathways. Although the range of mechanisms of immune dysregulation leading to renal disease is broad, the pathways leading to injury are similar. Loss of immune homeostasis in renal disease results in perpetual immune cell recruitment and worsening damage to the kidney. Uncoordinated attempts at tissue repair, after immune-mediated disease or non-immune mediated injury, result in fibrosis of structures important for renal function, leading eventually to kidney failure. As renal disease often manifests clinically only when substantial damage has already occurred, new diagnostic methods and indeed treatments must be identified to inhibit further progression and promote appropriate tissue repair. Studying cases in which immune homeostasis is re-established may reveal new treatment possibilities.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/cei.13119

The role of the immune system in kidney disease.

Objective. Some patients with systemic lupus erythematosus (SLE) are clinically quiescent despite persistent serologic activity. We determined the frequency of serologically active clinically quiescent (SACQ) SLE and its outcomes in prospectively followed patients with SLE. Methods. Patients with SLE followed between July 1970 and April 2008 with visits ≤ 18 months apart were identified. SACQ was defined as a ≥ 2-year sustained period without clinical activity with persistent serologic activity (increased anti-dsDNA and/or hypocomplementemia), during which antimalarials but neither steroids nor immunosuppressives were permissible. Characteristics of patients with an SACQ period and its features were analyzed. To determine flare predictors, anti-dsDNA and complement levels in SACQ patients who experienced flare were compared to levels in those who did not. Descriptive statistics were used; comparisons were made using t tests and chi-squared tests. Results. Of the patients studied, 56/924 (6.1%) were SACQ. They differed significantly from the non-SACQ SLE population only in the presenting SLE Disease Activity Index 2000 (7.34 vs 10.1 in non-SACQ), and frequency of steroid use (33.9% vs 60.8% in non-SACQ) and immunosuppressive use (3.6% vs 19.4% in non-SACQ) at first visit. Median SACQ period was 158 weeks. Thirty-three (58.9%) patients who were SACQ experienced flare (at median 155 weeks), 6 (10.7%) became clinically and serologically quiescent (236 weeks), and 17 continued to be SACQ (159 weeks). Common flare manifestations were arthritis, mucous membrane involvement, and sterile pyuria. Fluctuations in anti-dsDNA or complement levels did not predict flare. Conclusion. Fifty-nine percent of SACQ patients experienced flare, but after a median of 3 years. Fluctuations in complement and anti-dsDNA levels did not predict flare, thus treatment decisions in these patients must rely upon close clinical observation. Alternative predictive biomarkers warrant study.

https://www.jrheum.org/content/jrheum/37/9/1822.full.pdf

Prolonged Serologically Active Clinically Quiescent Systemic Lupus Erythematosus: Frequency and Outcome

https://www.ajkd.org/article/S0272-6386(07)01559-4/pdf

Antinucleosome Antibodies as a Marker of Active Proliferative Lupus Nephritis

In systemic lupus erythematosus patients, a strong association between the occurrence of antibodies against complement C1q (anti-C1q) and lupus nephritis can be observed. However, the predictive value of anti-C1q titres for a renal flare remains to be determined. Increasing titres of anti-C1q before the occurrence of clinical apparent nephritis might not only serve as a clinical parameter but also indicate a direct pathogenic mechanism of anti-C1q.

/pdf/anti-c1q-autoantibodies-do-not-correlate-with-the-occurrence-84l6y88gz7.pdf

Anti-C1q autoantibodies do not correlate with the occurrence or severity of experimental lupus nephritis

Autoantibodies against complement C1q (anti-C1q Abs) were shown to strongly correlate with the occurrence of severe nephritis in patients with systemic lupus erythematosus (SLE), suggesting a potential pathogenic role by interfering with the complement cascade. To analyze the humoral immune response against C1q at the molecular level, we screened a bone marrow-derived IgGkappa/IgGlambda Fab phage display library from a SLE patient with high anti-C1q Ab titer against purified human C1q. Six Fabs that exhibited strong binding to C1q in ELISA were isolated. The anti-C1q Fabs recognized neoepitopes that were only exposed on bound C1q and not present on soluble C1q mapping to different regions of the collagen-like region of C1q. Analysis of the genes encoding the variable H and L chains of the IgG-derived anti-C1q Fab revealed that all the variable H and L chain regions were highly mutated, with nucleotide and amino acid homologies to the closest germline in the range of 71-97% (average 85 +/- 4) and 72-92% (average 88 +/- 6), respectively. In addition, the variable region of the Fabs exhibited high replacement to silent ratios. The six anti-C1q Fabs were shown to be of high affinity, with a K(d) ranging from of 8.4 x 10(-8) M to 1.4 x 10(-7) M, comparable to an antiviral immune response. Our data underlines the notion that the development of anti-C1q Abs in SLE is the consequence of an Ag-driven, affinity-matured immune response. Those anti-C1q Fabs are unique tools to address how complement C1q is implicated in the pathogenesis of SLE.

/pdf/autoantibodies-against-c1q-in-systemic-lupus-erythematosus-2cekjzte8x.pdf

Autoantibodies against C1q in Systemic Lupus Erythematosus Are Antigen-Driven

Background Life-threatening infections are a major cause of death after allogeneic stem cell transplantation. Complement Mannose-binding lectin is a key component of innate immunity. Functional deficiency of mannose-binding lectin due to genetic polymorphism is frequent. Previous reports showed conflicting results with respect to the influence of functional mannose-binding lectin deficiency on infectious risk after allogeneic stem cell transplantation. The aim of this study was to clarify the impact of low mannose-binding lectin levels on infectious risk in a unique cohort of very long-term survivors after stem cell transplantation.

Design and Methods Incidence of major infections was evaluable in 43 out of 44 very long-term survivors (over ten years) and studied retrospectively in relation to mannose-binding lectin serum concentrations.

Results Recipients with mannose-binding lectin levels below 1,000 ng/mL were at increased risk to suffer from one or more major infections ( P =0.002) during entire follow up. Infectious susceptibility was increased after neutrophil recovery, particularly until 24 months (Hazard Ratio 3.4) with sustained effects afterwards (Hazard Ratio 2.9). Mannose-binding lectin serum concentrations below 1,000 ng/mL were independently associated with major infections after neutrophil recovery ( P =0.009). In subgroup analyses occurrence of severe herpes virus infections in particular was associated with significantly lower mannose-binding lectin levels ( P =0.02).

Conclusions Our findings indicate that low mannose-binding lectin levels may predict markedly increased susceptibility to severe infections with sustained effects even late after allogeneic stem cell transplantation. Determinations of mannose-binding lectin status should therefore be included into pre-transplantation risk assessment.

Mannose-binding lectin levels and major infections in a cohort of very long-term survivors after allogeneic stem cell transplantation.

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Antinucleosome Antibodies as a Marker of Active Proliferative Lupus Nephritis

Anti-C1q autoantibodies do not correlate with the occurrence or severity of experimental lupus nephritis

Anti-C1q autoantibodies do not correlate with the occurrence or severity of experimental lupus nephritis

Autoantibodies against C1q in Systemic Lupus Erythematosus Are Antigen-Driven

Mannose-binding lectin levels and major infections in a cohort of very long-term survivors after allogeneic stem cell transplantation.